In renal phosphate‐wasting diseases characterized by inappropriately high circulating intact FGF23 such as X‐linked hypophosphatemia (XLH), autosomal dominant hypophosphatemic rickets (ADHR), or tumor‐induced osteomalacia (TIO), the FGF23‐mediated suppression of 1,25(OH)2D synthesis aggravates the hypophosphatemia, because in addition to renal phosphate wasting, 1,25(OH)2D‐mediated intestinal absorption of phosphate is reduced. This evidence concerns the gene FGF23 and autosomal dominant hypophosphatemic rickets.