Not surprisingly given the prevalence of RAS mutations in PDAC, early drug development efforts focused on targeting mutant KRAS and downstream RAS effectors, including Rapidly Accelerated Fibrosarcoma (RAF)/Mitogen Activated Protein Kinase (MEK)/Extracellular Signal-Regulated Kinases (ERK) and Phosphatidylinositol-4,5-bisphosphate 3-kinase (PI3K)/Protein Kinase B (AKT) signaling responsible for driving cancer cell proliferation and survival [23]. This evidence concerns the gene AKT1 and cancer.