While additional investigation is needed to understand the mechanism of FGF23 reduction in VillinCreERT2Cyp24fl/fl mice with kidney damage, these results support inhibition of intestinal CYP24A1 as an approach to mitigate secondary hyperparathyroidism and FGF23 excess in patients with CKD. The gene discussed is CYP24A1; the disease is secondary hyperparathyroidism.