NFKB1 and myelodysplastic syndrome: [7], [28] Stimulation of TLRs is known to lead to activation of intracellular pathways such as NF-kB and p38MAPK [3], which have both been documented as important molecular signals for tumorigenesis including in MDS [29], [30]. We recently report that TLR2 [26], the histone demethylase JMJD3 and multiple innate immune genes that are regulated by JMJD3 are overexpressed in BM CD34+ cells of MDS [31]. Of importance, JMJD3 is a known transcriptional target of TLR signaling stimulated NF-kB activity [32].