In line with our results in TET2MUT MDS patients, TET2 inhibition in DMOG treatment significantly reduced the percentage of KIR2D+ NK cells (p < 0.001, Fig. 3b), suggesting a role for TET2 in modulating the KIR expression on NK cells or the KIR2D+ subset proliferation. The gene discussed is KIR3DL1; the disease is myelodysplastic syndrome.