Considering that AMPK activity has been associated both with pro- and anti-tumorigenic effects depending on the cell type in which it is induced [55-57], our study sheds further light on the seemingly contradictory role of AMPK in tumor progression by demonstrating a specific requirement for AMPK in sustaining the antitumor activity of tumor-associated T cells. The gene discussed is PRKAA2; the disease is neoplasm.