Furthermore, α-SMA has been demonstrated to be a downstream protein of STAT1 [89], and inhibition of STAT1 signaling ameliorates tubulointerstitial fibrosis in diabetic kidney disease [63], attenuates pulmonary vascular fibrosis [62], and rescues the exacerbated remodeling in myocardial infarction [64]. This evidence concerns the gene ACTA1 and myocardial infarction.