Onset and progression of cancer in the liver rely on multifaceted molecular mechanisms entailing genetic and epigenetic alterations to oncogenes and tumor suppressor genes as well as disturbed control, anomalous function, and inappropriate interaction of crucial molecular cascades, such as Wnt/β-catenin, Hedgehog, MAPK, and PI3K/AKT/mTOR signaling pathways, with the circadian clock circuitry, overall favoring metaflammation, derangement of growth and differentiation control, and in due course carcinogenesis [35,36]. Here, AKT1 is linked to cancer.