In contrast, vitamin D-dependent rickets type 1 arises from CYP27B1 loss-of-function mutations that abolish 1α-hydroxylase activity, leading to deficient 1,25-dihydroxyvitamin D3 production, hypocalcemia, secondary hyperparathyroidism, and rickets [8,82]. The gene discussed is CYP27B1; the disease is secondary hyperparathyroidism.