NFKB1 and myelodysplastic syndrome: Tet2 LOF hematopoietic stem/progenitor cells (HSPCs) upregulated TLR-TRAF6 in response to inflammation, resulting in a shift from the canonical NF-κB pathway to the noncanonical NF-κB pathway, thereby avoiding inflammatory damage to mutated stem cells, and facilitating the Tet2 mutation-induced progression of myelodysplastic syndrome.142Dnmt3A LOF CHIP could also prevent hematopoietic stem cells from terminal differentiation through increasing methylation of IFNγ signaling pathways.143