During renal injury and chronic inflammation, increased secretion/expression of relevant enzymes and inflammatory mediators, and cytokines enable fibroblasts to differentiate towards myofibroblasts, the main responsible cells for renal fibrosis, and myofibroblast proliferation enables overexpression of α-smooth muscle actin (α-SMA), collagen (COL), fibronectin, and matrix metalloproteinases (MMP) [99–102]. This evidence concerns the gene ACTA1 and renal fibrosis.