AKT1 and neoplasm: In particular, stimulation of beta-adrenergic receptors has been shown to increase intracellular cAMP levels, leading to activation of downstream pathways via protein kinase A, which intersect with EGFR-mediated MAPK and PI3K–AKT signaling, thereby facilitating tumor cell proliferation, metastatic potential, and the development of resistance to anti-EGFR therapies.