Given that cytokine suppression is inefficient with ruxolitinib alone, more direct inhibition of MEK/ERK signaling, as well as other pathways such as NFκB, may antagonize the pro-inflammatory and disease-driving state in MPNs [42, 43], and perhaps the ruxolitinib persistent survival of MPN-driving cells. This evidence concerns the gene MAPK1 and myeloproliferative neoplasm.