In our research, we found that an anti-NKG2D blocking antibody markedly attenuated cytolysis by T cells treated with CML-RAE-1γ-Dex, suggesting that CML-RAE-1γ-Dex overcame poor antigen presentation efficiency and augmented the antitumor T-cell response via an NKG2D-dependent mechanism (Fig. 4b, c). The gene discussed is KLRK1; the disease is chronic myelogenous leukemia, BCR-ABL1 positive.