AKT1 and cancer: We hypothesize that the concomitant activation of PI3K/Akt (through insulin/IGF-1 and EGF receptors), PKD/ERK (via agonist-induced Gq signaling) and mTORC1 (synergistically through PI3K/Akt induced by insulin/IGF-1R and EGFR and GPCR-stimulated ERK/p90RSK) in PDAC cells potently stimulates DNA synthesis and proliferation of these cancer cells, and thus provide potential targets for chemotherapeutic intervention (Figure 2).