Dnmt3a loss increased the release of pro-inflammatory mediators, especially when combined with oncogenes such as FLT3-ITD and NRas. Some alternations in gene expression that are able to activate TNFa signaling and pro-inflammatory gene expression as reported in the JAK2V617F/Dnmt3a double-mutant animals were also demonstrated in primary cells from MPN subjects with vs. without mutated DNMT3A [94]. Here, DNMT3A is linked to myeloproliferative disorder.