A study using mouse models with cardio-renal syndrome post-myocardial infarction showed that elevated FGF-23 levels were associated with a profibrotic effect on renal and cardiac levels, through the binding between FGF-23 and its receptor FGFR4 in the kidney that induces β-catenin signaling pathway activation; however, this effect was reduced if an FGFR antagonist was administered [47]. This evidence concerns the gene FGFR4 and myocardial infarction.