proposed on this basis that the TIM-3/Gal-9 signaling axis and imbalanced bone marrow microenvironment not only contribute to the pathogenesis of MDS, but also accelerates the transition of MDS to secondary AML (sAML) by inducing proliferation of progenitor cells and immune escape and thereby accelerating MDS) transformation (27). This evidence concerns the gene HAVCR2 and myelodysplastic syndrome.