Moreover, with the growing understanding of inflammasome pathway pathology and their role in promoting self-renewed inflammation that can develop into cellular death and disruption of normal hematopoiesis [41], targeting key signaling mediators such as IRAK1 and IRAK4, as well as ligands and receptors, including S100A9, CD33, IL-1RAP, TGF-β and IL1B, has laid the groundwork for new immune-based treatment of MDS [9]. The gene discussed is S100A9; the disease is myelodysplastic syndrome.