Moreover, the acute incubation of Wt and Nod1−/− cardiomyocytes with FGF-23 induced a similar systolic and diastolic Ca2+ mishandling (Supplementary Figure S2), suggesting that probably NOD-1 and the FGF-23 axis are involved in independent pathways that contribute to the regulation of Ca2+ handling, at least in our experimental model of CKD. Here, FGF23 is linked to chronic kidney disease.