Some researchers have proposed dividing HCC into two molecular subtypes, each accounting for approximately 50% of the disease: the proliferation class, driven by PI3K-AKT-mTOR, RAS-MAPK, and MET signaling, and the non-proliferation class, often associated with Wnt/β-catenin signaling pathway activation and immune exclusion, often due to CTNNB1 mutations (encoding β-catenin) [8, 36, 37, 47, 48]. This evidence concerns the gene AKT1 and hepatocellular carcinoma.