Regarding the implication of NK cells in TFR, individuals who controlled CML after imatinib therapy cessation showed higher NK cytotoxic function towards the target K562 cell line, lacking HLA class I. Furthermore, NKG2D gene polymorphisms [58] and the IFN-γ and TNF-α cytokine secretion by NK (CD56dimCD16−) cells correlated with the successful drug discontinuation and control of CML [57,59]. The gene discussed is TNF; the disease is chronic myelogenous leukemia, BCR-ABL1 positive.