In myocardial fibrosis caused by myocardial injury, the N-terminal peptide C0–C1f of the myocardial binding protein C can activate the NF-κB pathway through TLR4 to cause inflammation and delay TGF-β-induced fibroblast activation; miR-146 can inhibit the C0-C1f function [66]. This evidence concerns the gene TGFB1 and Myocardial fibrosis.