In the case of NASH-related HCC, intracellular lipid accumulation with potential lipotoxicity [15,16], alterations in the control of cell cycle and apoptosis [17], disruption of the peroxisome proliferator-activated receptor-γ (PPAR-g) coactivators [18] have been all proposed as factors enhancing the inflammatory damage and potentially contributing to the liver remodelling and fibrosis. The gene discussed is PPARG; the disease is metabolic dysfunction-associated steatohepatitis.