The NK cell killing ability is controlled by a fine-tuned signaling balance induced by NK activating receptors (including NKG2D) binding to their ligands on tumor cells, and by NK inhibitory receptors recognizing MHC class I. In cancer, expression of NKG2D ligands, such as UL16-binding proteins can be modulated at the transcriptional level, notably by IFNγ, DNA methylation, or low histone acetylation, and at the translational level, mostly through microRNAs [77,78]. The gene discussed is KLRK1; the disease is cancer.