The findings by us and others that kl/kl mice develop skeletal muscle atrophy and wasting [63,64,65,66,67,68] and that deletion of the renal phosphate transporter NaPi-2a in kl/kl mice reduces serum phosphate levels and protects from skeletal muscle atrophy [63] suggest that pathologic changes are not directly caused by the absence of klotho but indirectly by other pathologic changes that occur in the absence of klotho, such as hyperphosphatemia [63]. The gene discussed is SLC34A1; the disease is muscle atrophy.