Recently, FGF23 has been found to promote fibrosis in injury-primed renal fibroblasts through activation of both TGFβ/Smad and FGFR4/PLCγ/calcineurin/NFAT signaling [60,61], and to cause cardiac fibrosis by upregulating β-catenin and TGFβ in vitro and after myocardial infarction in vivo [34]. This evidence concerns the gene FGF23 and myocardial infarction.