When a lack of glucose or glutamine is present, cancer cells can activate oncogenes, such as cMyc, by regulating the expression of metabolic enzymes PHGDHP, SAT1, and PSPH in the serine synthesis pathway; by using the remaining glutamine or glucose support serine from synthetic approaches; and by maintaining REDOX steady-state support, such as tumor cell survival in nutritional stress conditions [48]. The gene discussed is MYC; the disease is neoplasm.