We assume that the main effect is mediated at the molecular level through the induction of hepatic miRNAs (miR-22, miR-29c, and miR-219a) which may inhibit the expression of their targets including the main genes involved in the pathogenesis of liver fibrosis (including TGFβR1, COL3A1, and TGFβR2) and the inflammatory mediators resulting in boosting antioxidant potential, inhibition of fibro-genesis and improving hepatocyte structure and functions. The gene discussed is TGFBR2; the disease is Hepatic fibrosis.