PSPH and cancer: 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.