Huang et al. demonstrated that myocardial energy metabolism dysfunction induced by the IRF1-PGC1α axisplays a crucial role in the pathogenesis of type 4 CRS and suggested that hyperphosphatemia management or targeted intervention on HP-mediated IRF1 elevation and PGC1α downregulation could represent a future treatment able to reduce cardiovascular risk in CKD patients [6]. This evidence concerns the gene PPARGC1A and hyperphosphatemia.