Since CD33 CAR-NK cell efficacy could be limited by inhibitory receptors expressed in human NK cells (such as NKG2A) and their targets expressed on leukemic blasts (such as HLA.E), Bexte et al. generated CD33 CAR-NK cells combined with CRISPR/Cas9-mediated gene disruption of the NKG2A-encoding KLRL1 gene; the CD33 CAR-NK-gene edited cells displayed potent anti-leukemic cell activity and transcriptional activation following AML exposure [49]. Here, KLRC1 is linked to acute myeloid leukemia.