Since at least CD16A-independent NK cell cytotoxicity is often impaired in AML patients due to disease-related cellular defects29–31, we subsequently investigated whether AFM28 can induce anti-leukemic activity by AML patients’ residual endogenous innate immunity in cultures of freshly-drawn peripheral blood (PB) samples from newly diagnosed AML patients (n = 6), suggestive for the single-agent efficacy potential of AFM28 in AML patients. Here, FCGR3A is linked to acute myeloid leukemia.