Furthermore, studies have shown that histone lysine demethylases KDM3A and KDM3C bind the Timp1-promoter, a biomarker with profibrotic function [76,77], and stimulate its transcriptional activity, leading to activation of cardiac fibroblasts and induction of myocardial fibrosis [71,78], while KDM5B suppresses the expression of the activating transcription factor 3 (ATF3), an antifibrotic regulator of cardiac fibrosis, and stimulates the TGF-β signaling pathway and the subsequent increased expression of profibrotic genes [79]. This evidence concerns the gene TGFB1 and Myocardial fibrosis.