Mechanistic studies indicates that quercetin exerts multi-targeted effects in HCC models: it induces cell-cycle arrest at multiple checkpoints (G0/G1, S, G2/M), suppresses proliferative and invasive signaling (PI3K/Akt/mTOR, MAPK/ERK, NF-κB, JAK2/STAT3), activates the intrinsic (mitochondria-dependent) apoptotic cascade through downregulation of Bcl-2 family members, and modulates autophagy—where excessive autophagic activation can culminate in programmed cell death [15,16,17,18,19]. Here, AKT1 is linked to hepatocellular carcinoma.