During this activation process, HSC acquire a myofibroblast-like phenotype, transdifferentiating into myofibroblasts, and participate in liver fibrosis formation by proliferating and secreting ECM components, thus increasing the expression of α-smooth muscle actin (α-SMA) and type I collagen alpha 1 (Col1α1). The gene discussed is COL1A1; the disease is Hepatic fibrosis.