In summary, our findings constitutes an additional paradigm of eEF2K as a suppressor of carcinogenesis other than a role of cytoprotection in lung cancer cells, and delineate a novel mechanism underlying regulation of proliferation by eEF2K-mediated PKM2 phosphorylation and subsequent dimerization, leading to inhibit STAT3 phosphorylation and c-Myc expression accompanied by collapse of aerobic glycolysis (Fig. 7d). The gene discussed is MYC; the disease is lung cancer.