Indeed, Tim-3 expression is increased on blasts and in high-risk hematological diseases (Asayama T et al., 2017), together with its pathway companion, galectin-9, and proliferation of Tim-3+ MDS blasts can be inhibited by anti-Tim-3 antibody (Gonçalves Silva I et al., 2017; Wolf Y et al., 2020). Here, HAVCR2 is linked to hematologic disorder.