The findings presented demonstrate that the combined use of the PIM‐2 inhibitor SMI‐16a and the PARP1 inhibitor ABT888 leads to greater DNA damage compared to SMI‐16a alone, thereby facilitating NK cell cytotoxicity through the NKG2D/MICA signaling axis and inducing apoptosis in multiple myeloma cells. The gene discussed is KLRK1; the disease is AL amyloidosis.