Activation of TLR–TRAF6 signaling by chronic inflammation in myelodysplastic syndromes increases the competitive advantage of HSPCs harboring MDS mutations through the upregulation of the ubiquitin-modifying enzyme A20 and a switch from canonical to non-canonical NF-κB signaling.
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The authors declare no competing interests.
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Ueda, K., Kumari, R. & Steidl, U. Fueling clonal dominance through TRAFficking of NF-κB signaling. Nat Immunol 21, 489–490 (2020). https://doi.org/10.1038/s41590-020-0662-0