The clinical, biochemical, and genetic features of both FGF23-dependent and -independent forms of HR are discussed, including X-linked hypophosphatemia (XLH), autosomal dominant hypophosphatemic rickets (ADHR), autosomal recessive hypophosphatemic rickets (ARHR), tumor-induced osteomalacia (TIO), hereditary hypophosphatemic rickets with hypercalciuria (HHRH), and Fanconi syndrome. This evidence concerns the gene FGF23 and Fanconi renotubular syndrome.