It is likely that, among the oxygen-exposed cancer cells, which are subject to the Warburg effect and which are subject to the reverse Warburg effect is dependent on the expression levels of the oncogenes c-Myc, HIF-1α, and mutant p53, relative activities of LDH-A versus LDH-B, and the levels of other regulatory mechanisms that facilitate “aerobic glycolysis”. Here, HIF1A is linked to cancer.