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]. Here, CYP27B1 is linked to Hypocalcemia.