In the light of defense against free radicals, SIL rebalanced the high fatty acids catabolism in response to lipids accumulation and oxidative stress induced by lipids peroxidation via peroxisome proliferator-activated receptors (PPARs) and nuclear factor kappa B (NF-κB) pathways.[30,31] Additionally, SIL possesses the capacities to stabilize the hepatocyte membrane structure and manipulate the membrane permeability in the presence of the toxicity, as well as to retard the transformation from hepatic stellate cell to myofibroblasts resulting in liver fibrosis and cirrhosis.[32,33]. The gene discussed is NFKB1; the disease is Cirrhosis.