In addition, genetic deletion of ampkα1-coding gene, prkaa1 antagonized M-MDSC differentiation to macrophages and re-routed M-MDSC, but not G-MDSC, into cells that elicited direct antitumor cytotoxic effects through NOS2-mediated actions, suggesting the therapeutic use of AMPK inhibitors to overcome MDSC-induced T-cell dysfunction and AMPK inhibition as a potential therapeutic strategy to restore protective myelopoiesis in cancer. Here, PRKAA1 is linked to cancer.