In light of the pivotal underlying mechanisms of myocardial fibrosis validated by the fibroblast-specific, in vivo model (7), the particular focus herein is on the TGF-β and mitogen-activated kinases (MAPKs) pathways, which are evidenced targets by renalase (11, 13, 16, 17, 21, 68, 69), as presented in Figure 1. This evidence concerns the gene TGFB1 and Myocardial fibrosis.