Our team found that TIM-3 expression was significantly upregulated in Th1, Th17 and regulatory T cells (Treg) in MDS patients, and, of particular importance, TIM-3+ Treg cells exhibited dysfunction and their TGF-β secretion capacity was reduced (30), suggesting that TIM-3 may weaken the inhibitory capacity of Treg on effector T cells by altering its cytokine profile and while enhancing the overall immunosuppressive microenvironment and playing an important role in immune escape. This evidence concerns the gene HAVCR2 and myelodysplastic syndrome.