Similarities between the TRAF6-induced mouse hematopoietic phenotype and human del(5q) MDS strongly suggest that down-regulation of miR-146a in HSPCs plays a critical role in the development of MDS, largely by inhibiting TRAF6. As TRAF proteins are key intermediaries in the activation of canonical NF-kB signaling pathway (Bradley and Pober, 2001), these data suggest that NF-kB may be downstream of miR-146a and responsible for mediating a significant part of the miR-146a phenotype. The gene discussed is TRAF6; the disease is myelodysplastic syndrome.