GRP stimulation markedly increased the phosphorylation of Akt at Ser473 and ERK1/2 at Thr202/Tyr204, consistent with the activation of the PI3K/Akt and MAPK/ERK pathways, which are known to promote tumour cell proliferation, survival, and resistance to apoptosis [20,21]. The gene discussed is AKT1; the disease is neoplasm.