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Notably, percentages of TM-expressing classical monocytes were increased in patients with lower blast counts and in patients with ring sideroblasts (erythroblasts with mitochondrial iron accumulation) ( S100A8 mediator) and pre-mRNA splicing in MDS patients with SF3B1 -K700E mutations, resulting in the upregulation of pro-inflammatory signaling pathways ( SF3B1 mutations have been linked to over-activation of nuclear factor kappa B (NF-B) signaling and increased production of inflammatory cytokines (114)