Renal fibrosis mainly stems from abnormal activation of myofibroblasts and their secretion of large amounts of ECM, such as α-smooth muscle actin (α-SMA), fibronectin (FN), and large deposits of collagen type I (collagen I), causing abnormal expansion of the renal tubular mesenchyme (Figure 1) (Humphreys, 2018). The gene discussed is ACTA1; the disease is renal fibrosis.