A marker of cellular starvation, AMPK activation, is not usually observed in tumor cells and, in fact, tumor cells are highly anabolic, as seen by activation of the target of rapamycin (mTORC1 and mTORC2) in a majority of malignant cells.73, 74 Tumor cells derive ATP and other raw materials from anabolism by increased glutamine uptake, beta oxidation of fatty acids, and macropinocytosis, which is commonly seen in ras-transformed cells and is inhibited by rac1 activation.75, 76 Thus, carcinogenesis is not an energy-deficient state, but a state of altered substrate use, which can be targeted. The gene discussed is RAC1; the disease is neoplasm.