Class IA phosphatidylinositol-3 kinases (PI3Ks) together with AKT and mammalian target of rapamycin (mTOR) comprise the central axis of a complex, interconnected signaling network that integrates signals from growth factors, insulin, nutrients and oxygen to play a critical role in controlling cell growth, proliferation, metabolism, survival, and tumor angiogenesis. De-regulation of these processes is a required hallmark of cancer1 and aberrant activation of the class IA PI3K signaling occurs frequently in many malignancies including non-small cell lung cancer (NSCLC).
