In addition to 1,25(OH)2 vitamin D3, CYP24A1 also inactivates its precursor 25(OH) vitamin D. Homozygous pathogenic variants in CYP24A1 cause idiopathic infantile hypercalcemia, a condition first described in children undergoing vitamin D supplementation characterized by failure to thrive, dehydration, hypercalcemia, and nephrocalcinosis.9 This evidence concerns the gene CYP24A1 and nephrocalcinosis.