One possible explanation for the difference between high and low malignancy cells would be the inability of the low malignancy cells to increase AMPKα and ACC gene expression in response to OA.Thus, it is possible that the long-term effects promoted by the constitutive AMPK activation support the adaptation of metastatic cells to the energy pathways that are predominant in specific metabolic stress and that contribute to the growth advantage of tumour cells. The gene discussed is PRKAA1; the disease is neoplasm.