The genetic basis of XLH is a loss-of-function mutation in the PHEX gene (Phosphate regulating gene with Homology to Endopeptidases on the X chromosome) located at Xp22.1-p22.2 [2], which leads, through a not fully understood mechanism, to enhanced production of the phosphaturic hormone FGF23 by osteocytes as primary source, determining a selective renal phosphate wasting. The gene discussed is PHEX; the disease is X-linked dominant hypophosphatemic rickets.