On the other hand, an oncogenic role of JMJD3 has been documented in the case of T-cell acute lymphocytic leukemia (T-ALL) and myelodysplastic syndrome (MDS) [45, 46], which was largely attributed to its specific partnership with NF-κB and NOTCH, two transcription factors whose overactivations are highly associated with the induction of multiple types of inflammatory cytokines and the proliferation of T cells. This evidence concerns the gene NFKB1 and myelodysplastic syndrome.