Our data show for the first time that (a) olaparib significantly increased tumor cell sensitivity to NK-mediated killing and ADCC in both BRCA WT and BRCA mutant prostate carcinoma cells, independent of PD-L1 or epithelial growth factor receptor (EGFR) modulation; (b) olaparib treatment significantly enhanced NK killing in a variety of tumor types, including prostate, breast, and non-small cell lung carcinoma as well as chordoma; and (c) mechanistically, treatment with olaparib upregulated death receptor TRAIL-R2. Here, EGFR is linked to neoplasm.