On the basis of these data, we propose the following as the mechanism of action model for NSLC01 (Fig. 6): NSLC01 selectively activates eEF2K by inhibiting its phosphorylation at S366; activated eEF2K then phosphorylates the downstream eEF2 at T56, thus inhibiting its translation elongation function; this inhibition of translation reduces the availability of enzymes (ASNS, GHPDH, PSAT1, and PSPH) that drive the synthesis of asparagine, and likely, serine, necessary for cancer cell survival and proliferation. The gene discussed is ASNS; the disease is cancer.