This controversy has been fueled by a recent study showing that treatment of maintenance hemodialysis patients with secondary hyperparathyroidism and left ventricular hypertrophy with a vitamin D analog increased circulating intact FGF23 and aggravated left ventricular hypertrophy relative to a group treated with a calcimimetic that lowered circulating FGF23.(76) These findings support the notion that treatment of CKD patients with vitamin D analogs at the expense of increased FGF23 secretion may have untoward effects on cardiovascular endpoints. The gene discussed is FGF23; the disease is secondary hyperparathyroidism.