In the BM of MDS patients, it was demonstrated that more MDSCs (Lin−HLA−DR–CD33+) accumulated compared with healthy donor, the interaction of CD33 with receptor S100A9 (bind to surface glycoprotein receptors on MDSC) promoted MDSCs and induced IL-10 and TGF-β secretion, while early forced maturation of MDSCs rescued the hematologic phenotype of MDS [54]. The gene discussed is TGFB1; the disease is myelodysplastic syndrome.