In line with these data, transgenic uremic mice overexpressing α-Klotho exhibited less calcification than wild-type uremic mice [92], and exposure to soluble α-Klotho suppressed the high-Pi-induced osteogenic VSMC transition and subsequent mineralization in vitro [92]—suggesting the existence of vascular resistance to FGF-23 in CKD because of a concomitant vascular α-Klotho deficiency. This evidence concerns the gene KL and chronic kidney disease.