Excessive glucose, lipid and insulin-generated metabolites may disrupt the epigenetic balance, thereby altering transcriptional networks involved in redox homeostasis, peroxisome and mitochondria function, inflammation, insulin sensibility and lipid homeostasis, driving NAFLD development and NAFLD-associated HCC tumorigenesis (126, 128). Here, INS is linked to metabolic dysfunction-associated steatotic liver disease.