When stimulated by hepatic injury and inflammatory responses, HSCs transform from a quiescent to a highly proliferative and contractile myofibroblast phenotype, secreting large amounts of ECM proteins, releasing a series of pro-inflammatory factors (e.g., IL-6, etc.)and pro-fibrotic factors (e.g., TGF-β1) [6], overexpressing α-SMA, fibronectin, collagen and other proteins, which promote the progression of HF [7]. This evidence concerns the gene ACTA1 and hydrops fetalis.