AngII, TGFβ1, endothelin-1 (ET-1), other chemicals, and mechanical stimuli modulate cardiac fibrosis, which thereafter activate the signaling axes including canonical TGFβ/Smads, non-canonical TGFβ/MAPKs, actin cytoskeleton, and calcium dependent pathways, and thus result in the activation and differentiation of fibroblasts (Moustakas and Heldin, 2009; Sciarretta et al., 2009; Teekakirikul et al., 2010; Stempien-Otero et al., 2016). This evidence concerns the gene AGT and fibrosis.