Upon activation by diseases such as myocardial infarction, cardiac fibroblasts will proliferate and differentiate into myofibroblasts with high expression of α-smooth Muscle Actin (α-SMA), resulting in excessive deposition of ECM such as Collagen I and Collagen III in fibrotic myocardium [26,27]. Here, ACTA1 is linked to myocardial infarction.