We postulate that the basal level of AMPK activity, which is important for bioenergetic homeostasis of proliferation-active cells, is likely to be beneficial for tumor growth at large whereas a high or prolonged catabolic AMPK activity generates an imminent conflict with the expression of oncogenes, such as MYC, which drive strongly anabolic growth promoting pathways. The gene discussed is MYC; the disease is neoplasm.