Individuals with GACI who survive infancy have been reported to progress to autosomal recessive hypophosphatemic rickets type 2 (ARHR2).(14, 15) ARHR2 manifests clinically as short stature and bone deformities and is associated with ENPP1 variants, but it has not been reported to be associated with ABCC6 variants.(16, 17, 18, 19, 20) GACI survivors have been found to have elevated fibroblast growth factor 23 (FGF23), and this may contribute to the hypophosphatemic rickets and osteomalacia.(4, 16, 17). This evidence concerns the gene FGF23 and arterial calcification, generalized, of infancy, 1.