Biallelic loss‐of‐function variants in GALNT3 cause disorders of phosphate homeostasis, specifically hyperphosphatemic FTC and HHS,(86) acting through the FGF23 pathway.(63, 87) Although heterozygous carriers of FTC/HHS‐associated GALNT3 variants do not show any clinical features of FTC or HHS,(61) subtle biochemical abnormalities, including slightly elevated phosphate concentrations, have been reported.(41, 56). The gene discussed is FGF23; the disease is hypotrichosis 1.