SESN2 and cancer: Overexpression of SESN2 or SESN3 could inhibit NK-92 cell-mediated cytotoxic activation through the activation of AMPK and the suppression of mTORC1, which manifested as decreases in the natural cytotoxicity receptors (NKp44 and NKG2D) and cytotoxic factor (TNF-α) and weakened the antitumor activity of NK-92 cells, emphasizing the potential effect of SESNs on immunotherapy in cancer.