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| Pituitary hormone deficiency v4.5 | TTC26 |
Ida Ertmanska changed review comment from: PMID: 31595528 Shaheen et al., 2020 Report of seven individuals from seven families with syndromic ciliopathy clinical features, including severe neonatal cholestasis (lethal in one, required liver transplant in two cases). Other features: polydactyly (5/7), echogenic kidneys with impaired renal function (5/7), variable cardiac anomalies (5/7). TTC26 variants detected: NM_024926.4: c.788A>G, p.Asn263Ser (4 patients, shared haplotype); c.1331C>T, p.Pro444Leu (1 patient, and c.4-1G>C (2 patients). PMID: 32617964 David et al., 2020 Four patients from two apparently unrelated consanguineous Bedouin families with ciliopathy due to a homozygous TTC26 c.695A>G p.Asn232Ser mutation. Patients had dysmorphic features, early-onset cholestatic jaundice (4/4), pituitary hormone deficiency (2/4), postaxial polydactyly (3/4), ectopic / absent neurohypophysis (posterior lobe of the pituitary gland) on brain MRI (3/4). PMID: 34177428 Alfadhel et al., 2021 Nonconsanguineous Saudi family. The female proband exhibited cholestasis, cystic dilatation of intrahepatic biliary ducts, diabetes insipidus, dysmorphic facial features, optic atrophy, hydrocephalus, aqueductal stenosis, hyperextensible knee joints, bilateral knee dislocation, polydactyly, and syndactyly. Brain MRI showed pituitary hypoplasia. She died at 15 months of age. WGS + Sanger sequencing revealed a homozygous TTC26 variant (c.4-1G>C; NM_024926.3). PMID: 38135897 Papingi et al., 2024 Male patient with hexadactyly, pituitary stalk interruption, hepatopathy, nephropathy, unilateral hearing impairment, a congenital heart defect, and a bilateral lip-palate cleft. He was homozygous for TTC26 c.1006-5T> C. Parents are first degree-cousins, Afghan ancestry. PMID: 39514123 Yang et al., 2025 Chinese case of BRENS syndrome who exhibited bilateral small kidney size and abnormal kidney function, cryptorchidism and short penis, optic atrophy, pituitary anomalies, hexadactyly, congenital cardiac defect, thyroid dysfunction, partial hypopituitarism, and other features (though no biliary involvement). 3 TTC26 variant detected: c.1069+5G>A inherited from the mother and c.511A>G (p.Ile171Val) and c.1099T>C (p.Ser367Pro) from the father. Functional evidence: PMID: 24596149 Ishikawa et al., 2014 - Knockdown of ttc26 in zebrafish embryos or mutation of Dyf13 (TTC26 ortholog) in C. reinhardtii produced short cilia with abnormal motility. TTC26 is associated with AR Biliary, renal, neurologic, and skeletal syndrome, OMIM:619534 (OMIM accessed 22nd Apr 2026). Sources: Literature; to: PMID: 31595528 Shaheen et al., 2020 Report of seven individuals from seven families with syndromic ciliopathy clinical features, including severe neonatal cholestasis (lethal in one, required liver transplant in two cases). Other features: polydactyly (5/7), echogenic kidneys with impaired renal function (5/7), variable cardiac anomalies (5/7). TTC26 variants detected: NM_024926.4: c.788A>G, p.Asn263Ser (4 patients, shared haplotype); c.1331C>T, p.Pro444Leu (1 patient, and c.4-1G>C (2 patients). PMID: 32617964 David et al., 2020 Four patients from two apparently unrelated consanguineous Bedouin families with ciliopathy due to a homozygous TTC26 c.695A>G p.Asn232Ser mutation. Patients had dysmorphic features, early-onset cholestatic jaundice (4/4), pituitary hormone deficiency (2/4), postaxial polydactyly (3/4), ectopic / absent neurohypophysis (posterior lobe of the pituitary gland) on brain MRI (3/4). PMID: 34177428 Alfadhel et al., 2021 Nonconsanguineous Saudi family. The female proband exhibited cholestasis, cystic dilatation of intrahepatic biliary ducts, diabetes insipidus, dysmorphic facial features, optic atrophy, hydrocephalus, aqueductal stenosis, hyperextensible knee joints, bilateral knee dislocation, polydactyly, and syndactyly. Brain MRI showed pituitary hypoplasia. She died at 15 months of age. WGS + Sanger sequencing revealed a homozygous TTC26 variant (c.4-1G>C; NM_024926.3). PMID: 38135897 Papingi et al., 2024 Male patient with hexadactyly, pituitary stalk interruption, hepatopathy, nephropathy, unilateral hearing impairment, a congenital heart defect, and a bilateral lip-palate cleft. He was homozygous for TTC26 c.1006-5T> C. Parents are first degree-cousins, Afghan ancestry. PMID: 39514123 Yang et al., 2025 Chinese case of BRENS syndrome who exhibited bilateral small kidney size and abnormal kidney function, cryptorchidism and short penis, optic atrophy, pituitary anomalies (including missing pituitary stalk on imaging), hexadactyly, congenital cardiac defect, thyroid dysfunction, partial hypopituitarism, and other features (though no biliary involvement). 3 TTC26 variant detected: c.1069+5G>A inherited from the mother and c.511A>G (p.Ile171Val) and c.1099T>C (p.Ser367Pro) from the father. Functional evidence: PMID: 24596149 Ishikawa et al., 2014 - Knockdown of ttc26 in zebrafish embryos or mutation of Dyf13 (TTC26 ortholog) in C. reinhardtii produced short cilia with abnormal motility. TTC26 is associated with AR Biliary, renal, neurologic, and skeletal syndrome, OMIM:619534 (OMIM accessed 22nd Apr 2026). Sources: Literature |
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| Pituitary hormone deficiency v4.5 | TTC26 |
Ida Ertmanska changed review comment from: PMID: 31595528 Shaheen et al., 2020 Report of seven individuals from seven families with syndromic ciliopathy clinical features, including severe neonatal cholestasis (lethal in one, required liver transplant in two cases). Other features: polydactyly (5/7), echogenic kidneys with impaired renal function (5/7), variable cardiac anomalies (5/7). TTC26 variants detected: NM_024926.4: c.788A>G, p.Asn263Ser (4 patients, shared haplotype); c.1331C>T, p.Pro444Leu (1 patient, and c.4-1G>C (2 patients). PMID: 32617964 David et al., 2020 Four patients from two apparently unrelated consanguineous Bedouin families with ciliopathy due to a homozygous TTC26 c.695A>G p.Asn232Ser mutation. Patients had dysmorphic features, early-onset cholestatic jaundice (4/4), pituitary hormone deficiency (2/4), postaxial polydactyly (3/4), ectopic / absent neurohypophysis (posterior lobe of the pituitary gland) on brain MRI (3/4). PMID: 34177428 Alfadhel et al., 2021 Nonconsanguineous Saudi family. The female proband exhibited cholestasis, cystic dilatation of intrahepatic biliary ducts, diabetes insipidus, dysmorphic facial features, optic atrophy, hydrocephalus, aqueductal stenosis, hyperextensible knee joints, bilateral knee dislocation, polydactyly, and syndactyly. Brain MRI showed pituitary hypoplasia. She died at 15 months of age. WGS + Sanger sequencing revealed a homozygous TTC26 variant (c.4-1G>C; NM_024926.3). PMID: 38135897 Papingi et al., 2024 Male patient with hexadactyly, pituitary stalk interruption, hepatopathy, nephropathy, unilateral hearing impairment, a congenital heart defect, and a bilateral lip-palate cleft. He was homozygous for TTC26 c.1006-5T> C. Parents are first degree-cousins, Afghan ancestry. PMID: 39514123 Yang et al., 2025 Chinese case of BRENS syndrome who presented with kidney, neurological, skeletal, and other features (no biliary involvement). 3 TTC26 variant detected: c.1069+5G>A inherited from the mother and c.511A>G (p.Ile171Val) and c.1099T>C (p.Ser367Pro) from the father. Functional evidence: PMID: 24596149 Ishikawa et al., 2014 - Knockdown of ttc26 in zebrafish embryos or mutation of Dyf13 (TTC26 ortholog) in C. reinhardtii produced short cilia with abnormal motility. TTC26 is associated with AR Biliary, renal, neurologic, and skeletal syndrome, OMIM:619534 (OMIM accessed 22nd Apr 2026). Sources: Literature; to: PMID: 31595528 Shaheen et al., 2020 Report of seven individuals from seven families with syndromic ciliopathy clinical features, including severe neonatal cholestasis (lethal in one, required liver transplant in two cases). Other features: polydactyly (5/7), echogenic kidneys with impaired renal function (5/7), variable cardiac anomalies (5/7). TTC26 variants detected: NM_024926.4: c.788A>G, p.Asn263Ser (4 patients, shared haplotype); c.1331C>T, p.Pro444Leu (1 patient, and c.4-1G>C (2 patients). PMID: 32617964 David et al., 2020 Four patients from two apparently unrelated consanguineous Bedouin families with ciliopathy due to a homozygous TTC26 c.695A>G p.Asn232Ser mutation. Patients had dysmorphic features, early-onset cholestatic jaundice (4/4), pituitary hormone deficiency (2/4), postaxial polydactyly (3/4), ectopic / absent neurohypophysis (posterior lobe of the pituitary gland) on brain MRI (3/4). PMID: 34177428 Alfadhel et al., 2021 Nonconsanguineous Saudi family. The female proband exhibited cholestasis, cystic dilatation of intrahepatic biliary ducts, diabetes insipidus, dysmorphic facial features, optic atrophy, hydrocephalus, aqueductal stenosis, hyperextensible knee joints, bilateral knee dislocation, polydactyly, and syndactyly. Brain MRI showed pituitary hypoplasia. She died at 15 months of age. WGS + Sanger sequencing revealed a homozygous TTC26 variant (c.4-1G>C; NM_024926.3). PMID: 38135897 Papingi et al., 2024 Male patient with hexadactyly, pituitary stalk interruption, hepatopathy, nephropathy, unilateral hearing impairment, a congenital heart defect, and a bilateral lip-palate cleft. He was homozygous for TTC26 c.1006-5T> C. Parents are first degree-cousins, Afghan ancestry. PMID: 39514123 Yang et al., 2025 Chinese case of BRENS syndrome who exhibited bilateral small kidney size and abnormal kidney function, cryptorchidism and short penis, optic atrophy, pituitary anomalies, hexadactyly, congenital cardiac defect, thyroid dysfunction, partial hypopituitarism, and other features (though no biliary involvement). 3 TTC26 variant detected: c.1069+5G>A inherited from the mother and c.511A>G (p.Ile171Val) and c.1099T>C (p.Ser367Pro) from the father. Functional evidence: PMID: 24596149 Ishikawa et al., 2014 - Knockdown of ttc26 in zebrafish embryos or mutation of Dyf13 (TTC26 ortholog) in C. reinhardtii produced short cilia with abnormal motility. TTC26 is associated with AR Biliary, renal, neurologic, and skeletal syndrome, OMIM:619534 (OMIM accessed 22nd Apr 2026). Sources: Literature |
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| Pituitary hormone deficiency v4.5 | TTC26 |
Ida Ertmanska changed review comment from: PMID: 31595528 Shaheen et al., 2020 Report of seven individuals from seven families with syndromic ciliopathy clinical features, including severe neonatal cholestasis (lethal in one, required liver transplant in two cases). Other features: polydactyly (5/7), echogenic kidneys with impaired renal function (5/7), variable cardiac anomalies (5/7). TTC26 variants detected: NM_024926.4: c.788A>G, p.Asn263Ser (4 patients, shared haplotype); c.1331C>T, p.Pro444Leu (1 patient, and c.4-1G>C (2 patients). PMID: 32617964 David et al., 2020 Four patients from two apparently unrelated consanguineous Bedouin families with ciliopathy due to a homozygous TTC26 c.695A>G p.Asn232Ser mutation. Patients had dysmorphic features, early-onset cholestatic jaundice (4/4), pituitary hormone deficiency (2/4), postaxial polydactyly (3/4), ectopic / absent neurohypophysis (posterior lobe of the pituitary gland) on brain MRI. PMID: 34177428 Alfadhel et al., 2021 Nonconsanguineous Saudi family. The female proband exhibited cholestasis, cystic dilatation of intrahepatic biliary ducts, diabetes insipidus, dysmorphic facial features, optic atrophy, hydrocephalus, aqueductal stenosis, hyperextensible knee joints, bilateral knee dislocation, polydactyly, and syndactyly. Brain MRI showed pituitary hypoplasia. She died at 15 months of age. WGS + Sanger sequencing revealed a homozygous TTC26 variant (c.4-1G>C; NM_024926.3). PMID: 38135897 Papingi et al., 2024 Male patient with hexadactyly, pituitary stalk interruption, hepatopathy, nephropathy, unilateral hearing impairment, a congenital heart defect, and a bilateral lip-palate cleft. He was homozygous for TTC26 c.1006-5T> C. Parents are first degree-cousins, Afghan ancestry. PMID: 39514123 Yang et al., 2025 Chinese case of BRENS syndrome who presented with kidney, neurological, skeletal, and other features (no biliary involvement). 3 TTC26 variant detected: c.1069+5G>A inherited from the mother and c.511A>G (p.Ile171Val) and c.1099T>C (p.Ser367Pro) from the father. Functional evidence: PMID: 24596149 Ishikawa et al., 2014 - Knockdown of ttc26 in zebrafish embryos or mutation of Dyf13 (TTC26 ortholog) in C. reinhardtii produced short cilia with abnormal motility. TTC26 is associated with AR Biliary, renal, neurologic, and skeletal syndrome, OMIM:619534 (OMIM accessed 22nd Apr 2026). Sources: Literature; to: PMID: 31595528 Shaheen et al., 2020 Report of seven individuals from seven families with syndromic ciliopathy clinical features, including severe neonatal cholestasis (lethal in one, required liver transplant in two cases). Other features: polydactyly (5/7), echogenic kidneys with impaired renal function (5/7), variable cardiac anomalies (5/7). TTC26 variants detected: NM_024926.4: c.788A>G, p.Asn263Ser (4 patients, shared haplotype); c.1331C>T, p.Pro444Leu (1 patient, and c.4-1G>C (2 patients). PMID: 32617964 David et al., 2020 Four patients from two apparently unrelated consanguineous Bedouin families with ciliopathy due to a homozygous TTC26 c.695A>G p.Asn232Ser mutation. Patients had dysmorphic features, early-onset cholestatic jaundice (4/4), pituitary hormone deficiency (2/4), postaxial polydactyly (3/4), ectopic / absent neurohypophysis (posterior lobe of the pituitary gland) on brain MRI (3/4). PMID: 34177428 Alfadhel et al., 2021 Nonconsanguineous Saudi family. The female proband exhibited cholestasis, cystic dilatation of intrahepatic biliary ducts, diabetes insipidus, dysmorphic facial features, optic atrophy, hydrocephalus, aqueductal stenosis, hyperextensible knee joints, bilateral knee dislocation, polydactyly, and syndactyly. Brain MRI showed pituitary hypoplasia. She died at 15 months of age. WGS + Sanger sequencing revealed a homozygous TTC26 variant (c.4-1G>C; NM_024926.3). PMID: 38135897 Papingi et al., 2024 Male patient with hexadactyly, pituitary stalk interruption, hepatopathy, nephropathy, unilateral hearing impairment, a congenital heart defect, and a bilateral lip-palate cleft. He was homozygous for TTC26 c.1006-5T> C. Parents are first degree-cousins, Afghan ancestry. PMID: 39514123 Yang et al., 2025 Chinese case of BRENS syndrome who presented with kidney, neurological, skeletal, and other features (no biliary involvement). 3 TTC26 variant detected: c.1069+5G>A inherited from the mother and c.511A>G (p.Ile171Val) and c.1099T>C (p.Ser367Pro) from the father. Functional evidence: PMID: 24596149 Ishikawa et al., 2014 - Knockdown of ttc26 in zebrafish embryos or mutation of Dyf13 (TTC26 ortholog) in C. reinhardtii produced short cilia with abnormal motility. TTC26 is associated with AR Biliary, renal, neurologic, and skeletal syndrome, OMIM:619534 (OMIM accessed 22nd Apr 2026). Sources: Literature |
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| Pituitary hormone deficiency v4.5 | TTC26 |
Ida Ertmanska gene: TTC26 was added gene: TTC26 was added to Pituitary hormone deficiency. Sources: Literature Q2_26_promote_green tags were added to gene: TTC26. Mode of inheritance for gene: TTC26 was set to BIALLELIC, autosomal or pseudoautosomal Publications for gene: TTC26 were set to 31595528; 32617964; 34177428; 38135897; 39514123 Phenotypes for gene: TTC26 were set to Biliary, renal, neurologic, and skeletal syndrome, OMIM:619534; biliary, renal, neurologic, and skeletal syndrome, MONDO:0859191 Review for gene: TTC26 was set to GREEN Added comment: PMID: 31595528 Shaheen et al., 2020 Report of seven individuals from seven families with syndromic ciliopathy clinical features, including severe neonatal cholestasis (lethal in one, required liver transplant in two cases). Other features: polydactyly (5/7), echogenic kidneys with impaired renal function (5/7), variable cardiac anomalies (5/7). TTC26 variants detected: NM_024926.4: c.788A>G, p.Asn263Ser (4 patients, shared haplotype); c.1331C>T, p.Pro444Leu (1 patient, and c.4-1G>C (2 patients). PMID: 32617964 David et al., 2020 Four patients from two apparently unrelated consanguineous Bedouin families with ciliopathy due to a homozygous TTC26 c.695A>G p.Asn232Ser mutation. Patients had dysmorphic features, early-onset cholestatic jaundice (4/4), pituitary hormone deficiency (2/4), postaxial polydactyly (3/4), ectopic / absent neurohypophysis (posterior lobe of the pituitary gland) on brain MRI. PMID: 34177428 Alfadhel et al., 2021 Nonconsanguineous Saudi family. The female proband exhibited cholestasis, cystic dilatation of intrahepatic biliary ducts, diabetes insipidus, dysmorphic facial features, optic atrophy, hydrocephalus, aqueductal stenosis, hyperextensible knee joints, bilateral knee dislocation, polydactyly, and syndactyly. Brain MRI showed pituitary hypoplasia. She died at 15 months of age. WGS + Sanger sequencing revealed a homozygous TTC26 variant (c.4-1G>C; NM_024926.3). PMID: 38135897 Papingi et al., 2024 Male patient with hexadactyly, pituitary stalk interruption, hepatopathy, nephropathy, unilateral hearing impairment, a congenital heart defect, and a bilateral lip-palate cleft. He was homozygous for TTC26 c.1006-5T> C. Parents are first degree-cousins, Afghan ancestry. PMID: 39514123 Yang et al., 2025 Chinese case of BRENS syndrome who presented with kidney, neurological, skeletal, and other features (no biliary involvement). 3 TTC26 variant detected: c.1069+5G>A inherited from the mother and c.511A>G (p.Ile171Val) and c.1099T>C (p.Ser367Pro) from the father. Functional evidence: PMID: 24596149 Ishikawa et al., 2014 - Knockdown of ttc26 in zebrafish embryos or mutation of Dyf13 (TTC26 ortholog) in C. reinhardtii produced short cilia with abnormal motility. TTC26 is associated with AR Biliary, renal, neurologic, and skeletal syndrome, OMIM:619534 (OMIM accessed 22nd Apr 2026). Sources: Literature |
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| Pituitary hormone deficiency v2.106 | BRAF |
Catherine Snow Tag Q3_22_rating was removed from gene: BRAF. Tag Q3_22_NHS_review was removed from gene: BRAF. |
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| Pituitary hormone deficiency v2.106 | BRAF | Catherine Snow reviewed gene: BRAF: Rating: GREEN; Mode of pathogenicity: ; Publications: ; Phenotypes: ; Mode of inheritance: | |||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||
| Pituitary hormone deficiency v2.105 | BRAF |
Catherine Snow Source Expert Review Green was added to BRAF. Source NHS GMS was added to BRAF. Rating Changed from Amber List (moderate evidence) to Green List (high evidence) |
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| Pituitary hormone deficiency v2.32 | BRAF | Eleanor Williams Classified gene: BRAF as Amber List (moderate evidence) | |||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||
| Pituitary hormone deficiency v2.32 | BRAF | Eleanor Williams Gene: braf has been classified as Amber List (Moderate Evidence). | |||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||
| Pituitary hormone deficiency v2.31 | BRAF |
Eleanor Williams Tag Q3_21_NHS_review was removed from gene: BRAF. Tag Q3_22_NHS_review tag was added to gene: BRAF. |
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| Pituitary hormone deficiency v2.31 | BRAF |
Eleanor Williams Tag Q3_21_NHS_review tag was added to gene: BRAF. Tag Q3_22_rating tag was added to gene: BRAF. |
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| Pituitary hormone deficiency v2.31 | BRAF | Eleanor Williams Classified gene: BRAF as Red List (low evidence) | |||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||
| Pituitary hormone deficiency v2.31 | BRAF | Eleanor Williams Added comment: Comment on list classification: Promoting from red to amber, but with a green recommendation following GMS review. 5 cases reported with functional data implicating pituitary hormone deficiencies. | |||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||
| Pituitary hormone deficiency v2.31 | BRAF | Eleanor Williams Gene: braf has been classified as Red List (Low Evidence). | |||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||
| Pituitary hormone deficiency v2.30 | BRAF | Eleanor Williams Phenotypes for gene: BRAF were changed from to Cardiofaciocutaneous syndrome, OMIM:115150; cardiofaciocutaneous syndrome, MONDO:0015280 | |||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||
| Pituitary hormone deficiency v2.29 | BRAF | Eleanor Williams Publications for gene: BRAF were set to | |||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||
| Pituitary hormone deficiency v2.28 | BRAF | Eleanor Williams Added comment: Comment on mode of pathogenicity: All missense, activating variants | |||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||
| Pituitary hormone deficiency v2.28 | BRAF | Eleanor Williams Mode of pathogenicity for gene: BRAF was changed from to Loss-of-function variants (as defined in pop up message) DO NOT cause this phenotype - please provide details in the comments | |||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||
| Pituitary hormone deficiency v2.27 | BRAF | Eleanor Williams Mode of inheritance for gene: BRAF was changed from to MONOALLELIC, autosomal or pseudoautosomal, imprinted status unknown | |||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||
| Pituitary hormone deficiency v2.26 | BRAF | Eleanor Williams edited their review of gene: BRAF: Added comment: PMID: 33795686 - Gualtieri et al 2021 - report 5 unrelated patients with 4 different missense variants in BRAF. WES did not find any other likely causative variants. They all had Cardio-Facio-Cutaneous (CFC) syndrome and were identified to have features of Septo-Optic Dysplasia (SOD). Functional studies using HEK293T cells showed that the BRAF genetic variants are pathogenic and result in activation of the ERK/MAPK pathway. Mice expressing one of the variants found BRAF p.Q257R showed abnormalities in terminal differentiation of hormone-producing cells.; Changed publications to: 33795686; Changed phenotypes to: Cardiofaciocutaneous syndrome, OMIM:115150, cardiofaciocutaneous syndrome, MONDO:0015280 | |||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||
| Pituitary hormone deficiency v2.15 | BRAF | Eleanor Williams reviewed gene: BRAF: Rating: ; Mode of pathogenicity: ; Publications: ; Phenotypes: CARDIOFACIOCUTANEOUS SYNDROME + HYPOPITUITARISM; Mode of inheritance: MONOALLELIC, autosomal or pseudoautosomal, imprinted status unknown | |||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||
| Pituitary hormone deficiency v2.14 | BRAF |
Eleanor Williams gene: BRAF was added gene: BRAF was added to Pituitary hormone deficiency. Sources: Expert review Mode of inheritance for gene: BRAF was set to |
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