Massive endeavors were made to relive or reverse myocardial fibrosis (Yang et al., 1999; Cunnington et al., 2009; Lei et al., 2011; Khalil et al., 2017), but the effect of those treatment strategies was failed because targeting TGF-β1, SMAD2/3, or TβRI/II directly will be ended up with poor outcomes like autoimmune diseases, heart failure, or unknown risks (Shull et al., 1992; Wang et al., 2005). This evidence concerns the gene TGFBR1 and autoimmune disease.