Previous findings have indicated that neovascularization, which is significantly increased during the development of liver fibrosis, as well as oxidative stress, cytokeratin (CK) 18 expression, IR, tumor necrosis factor-α (TNF-α) and adiponectin status play pivotal roles in the progression of NASH to HCC [7,8]. This evidence concerns the gene TNF and metabolic dysfunction-associated steatohepatitis.