Although the pathophysiological mechanism remains unclear, insulin resistance might influence hepatocarcinogenesis via several molecular pathways, such as phosphatase and tensin homolog (PTEN)/P13K/Akt and MAPK kinase (MAPKK).[30] Glucose abnormality might also be related to dysregulation of the insulin-like growth factor (IGF) system and the type-IIGF receptor (IGF-IR) signaling pathway, which is important for HCC development.[31] The knowledge of these pathways has important consequences in the goal of HCC treatment.[32–35]. This evidence concerns the gene AKT1 and hepatocellular carcinoma.