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]. This evidence concerns the gene SAT1 and cancer.