In conclusion, these findings collectively model the multiple roles of TIM3 in the pathogenesis of MDS, where TIM3 acts as a primitive cell-intrinsic regulator to promote malignant clonal proliferation and disrupts bone marrow microenvironmental homeostasis as well as promotes disease progression and accelerates leukemic transformation in conjunction with the ligand Gal-9. The gene discussed is HAVCR2; the disease is myelodysplastic syndrome.