By selectively retaining or upregulating non-classical MHC-I molecules (e.g., human leukocyte antigen-E) that interact with inhibitory receptors, i.e., immune checkpoint molecular pair CD94 (encoded by KLRD1) and NKG2A (encoded by KLRC1), and simultaneously decreasing classical MHC-I expression, tumor cells inhibit NK-mediated cytotoxicity and promote immune evasion [44,45]. This evidence concerns the gene KLRD1 and neoplasm.