AKT1 and neoplasm: Upon activation by their ligands, receptor tyrosine kinases such as EGFR or c-MET phosphorylate and inhibit GSK-3β activity via the downstream PI3K/AKT signaling axis, thereby preventing β-catenin degradation and promoting its nuclear entry, which achieves a direct convergence of growth factor signaling and the Wnt pathway to potently drive tumor cell proliferation and survival [121].