Given the strong associations of elevated PTH and FGF23 with bone disease, cardiovascular disease, and mortality (1, 5–7), further research should investigate the long-term effects of intestinal Cyp24a1 deletion on mineral homeostasis, skeletal histomorphometry, arterial calcification, and left ventricular hypertrophy in adenine-induced and other mouse models of CKD. The gene discussed is PTH; the disease is chronic kidney disease.