Although there are some discrepancies in ER stress-mediated biological functions according to the type of variants and their ER stress-inducing capacity, they can generally elicit ER stress-mediated biological responses such as ROS production, inflammatory cytokine production, TGF-β secretion, hepatocyte proliferation followed by apoptosis, and enhanced HBsAg secretion (in case of HBcAg variant), all of which are linked to the progression of liver disease. This evidence concerns the gene TGFB1 and liver disorder.