Quercetin also reduced stabilization of β-catenin and HIF-1α, induced activation of caspase-3, and inhibited Akt, mTOR, and ERK phosphorylation in cancers, denoting that quercetin facilitates the loss of cell viability, apoptosis, and autophagy through modulation of PI3K/Akt/mTOR, Wnt/β-catenin, and MAPK/ERK1/2 pathways [33, 34]. This evidence concerns the gene AKT1 and cancer.