Chronically enhanced insulin/IGF1 signaling has been found to promote pancreatic cancer cell proliferation and survival through both the insulin-like growth factor 1 receptor (IGF1R) and insulin receptor-mediated pathways, which activate the downstream phosphatidylinositol 3-kinase (PI3K), mammalian target of rapamycin (mTOR), and the mitogen-activated protein kinase (MAPK) signal pathways, as well as downregulating the tumor suppressor PTEN [45,46,47]. The gene discussed is IGF1R; the disease is pancreatic neoplasm.