In its pediatric form, patients who survive infancy or newly diagnosed children without a GACI phenotype, go on to develop fibroblast growth factor 23-mediated autosomal recessive hypophosphatemic rickets type 2 (ARHR2) with continued risk of calcification, cardiovascular complications, and hearing deficits [2,3,7]. This evidence concerns the gene FGF23 and hypophosphatemic rickets, autosomal recessive, 2.