Furthermore, FGF23 promotes myocardial fibrosis via activation of β-Catenin (Hao et al., 2016), activates the intra-cardiac renin-angiotensin-aldosterone system (RAAS), which in turn promotes LVH and cardiac fibrosis (Böckmann et al., 2019), and it is associated with endothelial dysfunction in CKD patients (Yilmaz et al., 2010), and in human coronary artery endothelial cells in vitro (Richter et al., 2016). This evidence concerns the gene FGF23 and chronic kidney disease.