Insulin has been suggested to influence tumor cell metabolism and anabolism by directing the utilization of glucose through PI3K-Akt signaling, leading to (1): enhanced glycolytic flux resulting in the generation of ATP (2); the promotion of aerobic glycolysis with the generation of lactate and the regeneration of NAD+ (3); increased production of ribose-5-phosphate, the precursor for purine and pyrimidine nucleotide synthesis, through the pentose phosphate pathway, and (4) increased lipid synthesis (162). The gene discussed is INS; the disease is neoplasm.