It is known that biallelic loss‐of‐function GALNT3 mutations cause the rare autosomal recessive disorder FTC and HHS in which deficient GALNT3‐mediated O‐glycosylation results in enhanced cleavage and inactivation of the phosphaturic hormone FGF23, leading to increased/normal inactive C terminal FG23, low intact FGF23, and hyperphosphatemia.(87) However, whether these rare variants alter BMD has not been assessed in most cases. The gene discussed is GALNT3; the disease is hyperphosphatemia.