Although there is ample knowledge of the specific mechanisms of action of BEZ235 and BKM120 on NSCLC [24–26], little is known about the metabolic responses to PI3K signaling impairment in NSCLC tumor cells with KRAS-G12C mutations, thus hampering the discovery of possible new metabolic targets with better drug responses. The gene discussed is KRAS; the disease is neoplasm.