Since both the ERK and PI3K pathways are effectors of KRAS, activating mutations of KRAS reinforce the crosstalk between insulin/IGF-1 receptor and GPCR signaling systems, thereby increasing the robustness of the network induced by insulin/IGF-1 and GPCR agonists in pancreatic cancer cells. The gene discussed is KRAS; the disease is pancreatic neoplasm.