It is worth mentioning that among potential molecular targets for cirrhosis therapy, one may distinguish the following: (1) hepatic stellate cells (HSCs) through pharmacological inhibitors of the TGF-β pathway, which is pivotal in HSC activation, can suppress fibrosis progression by preventing fibrogenic signaling [175,176]; (2) matrix metalloproteinases (MMPs) essential for extracellular matrix (ECM) degradation. This evidence concerns the gene TGFB1 and Cirrhosis.