There is verygood evidence that the severe phenotype of α-Klotho- andFgf23-deficient mice is due to uncontrolled production of1,25(OH)2D3 and subsequent chronic hypercalcemia andhyperphosphatemia because concomitant ablation of vitamin D signaling completely rescuesα-Klotho−/− and Fgf23−/− mice (Hesse et al. 2007; Anour et al.2012; Streicher et al.2012). Here, KL is linked to hypercalcemia disease.