In the case of T-ALL and MDS, an oncogenic role of JMJD3 has been well documented, which was largely attributed to its specific partnership with NF-κB and NOTCH15,21, two TFs whose overactivations are highly associated with the induction of multiple types of inflammatory cytokines and the proliferation of T cells3,40. This evidence concerns the gene KDM6B and myelodysplastic syndrome.