Therapeutically, given that many of the cellular and molecular components are important in driving the overall pathology, inhibition of p50 subunit of NF-κB, hyperactivated lymphocytes, IL-6 overproduction, and TRAF6 represent multiple opportunities for therapeutic intervention to disrupt the pathogenic process leading to myeloid malignancies, and combinatorial inhibition may have even greater therapeutic impact. Here, NFKB1 is linked to myeloid neoplasm.