However, clinical studies have clearly shown that hyperphosphatemia or increased PTH are not the drivers of FGF23 secretion in early stage CKD patients.(71) Circulating intact FGF23 is a strong and independent risk factor for CKD progression, left ventricular hypertrophy, and mortality in CKD patients,(72, 73, 74) and may directly promote left ventricular hypertrophy.(73, 75) It is clear that elevated FGF23 levels in CKD patients contribute to the suppression of 1,25(OH)2D production, which is already diminished due to the reduction in functional kidney mass. This evidence concerns the gene FGF23 and chronic kidney disease.