Acute myeloid leukemia (AML) is particularly susceptible to NK-cell cytotoxicity, providing a strong biological rationale to retarget NK cells against myeloid-associated antigens and thereby amplify intrinsic antileukemic activity; accordingly, CAR-NK constructs specific for CD33 and CD123 have shown robust activity in preclinical systems (35–37). The gene discussed is CD33; the disease is acute myeloid leukemia.