Subsequently, we have elucidated that TIM3 can regulate the formation of the immunosuppressive microenvironment in MDS through different ligand-dependent pathways: The TIM-3/Gal-9 signaling axis promotes myeloid-derived suppressor cell (MDSC) expansion and induces CD8+ T-cell functional depletion (17); whereas, TIM-3/CEACAM1 interaction, which in turn enhances the immunosuppressive capacity of MDSC, promotes secretion of inhibitory cytokines such as IL-10 and TGF-β, which ultimately exacerbates the bone marrow inflammatory microenvironment (18). This evidence concerns the gene HAVCR2 and myelodysplastic syndrome.