Although IL-6, initially considered as a hepatoprotective substance in liver steatosis, is capable of decreasing oxidative stress and averting mitochondrial dysfunction, it could also advance hepatic regeneration and repair, induce inflammation, sensitize the liver to injury, induce IR, stimulate hepatocyte apoptosis, and participate in NASH development [19]. This evidence concerns the gene IL6 and metabolic dysfunction-associated steatohepatitis.