However, the underlying pathological and physiological mechanisms linking T2DM to HCC are multifaceted, involving associations with various conditions such as NAFLD, heightened hepatic insulin resistance, hyperinsulinemia, activation of pro-inflammatory mediators, oxidative stress, JNK-1 activation, increased IGF-1 activity, alterations in gut microbiota, and immune regulation [17,18]. This evidence concerns the gene MAPK8 and Hyperinsulinemia.