The BCR-ABL1 tyrosine kinase inhibitors (TKIs) dramatically improved the long-term outcome of chronic myeloid leukemia (CML). Notably, a substantial subset of the patients who had achieved deep molecular response experienced treatment-free remission (TFR) even after discontinuation of TKIs, which indicates the possibility that TKIs may enable “cure” without any further consolidation therapy. However, response to TKIs is variable, the determinants of which is unclear. Given that NK cells in peripheral blood increase in the CML patients with good therapeutic responses, TKIs may induce antitumor immunity against CML cells. It has been shown that TKIs enhance antitumor immunity, and several reports including ours have implied that killer immunoglobulin-like receptor (KIR), highly polymorphic NK cell receptor, play important roles. The presence or absence of KIRs have been extensively discussed, but next-generation sequencing enables allelic genotyping of KIRs, which is now uncovering novel aspects of KIRs. Here we summarize genetic and immunological aspects of KIRs, and discuss the association between allelic polymorphisms of KIRs and CML.