KRAS mutated cancer cells, including NSCLC cells, display distinct metabolic reprogramming for cancer cell growth, proliferation, and survival [8–10] and can stimulate nutrient scavenger processes such as macropinocytosis and autophagy, which generate endogenous vesicles, macropinosomes, and autophagosome [11–13]. This evidence concerns the gene KRAS and non-small cell lung carcinoma.