Specifically, BIM sensitizes NK cell lines to chemotherapy-induced apoptosis, DAPK1 mediates p53-dependent apoptosis, SHP1, and SOCS6 inactivate the JAK/STAT signaling pathway, and TET2 silencing may contribute to early global hypermethylation in ENKTL, so it is easily understood how hypermethylation of multiple tumor suppressor promoters may create additive effects leading to tumor growth and malignant transformation [26]. This evidence concerns the gene TET2 and neoplasm.