Additionally, eEF2K promotes cancer cell survival, proliferation, and chemoresistance through mechanisms independent of translational control, including the activation of oncogenic signaling pathways such as c-Myc, cyclin D1, integrin β1, IGFR1B, PDL1, PP2A-A, and the PI3K/AKT/mTOR, STAT3, and SRC/FAK pathways [36–40]. This evidence concerns the gene STAT3 and cancer.