Consistent with our findings, high expression levels of galectin‐9 correlated with infiltration of TIM3+Treg in chronic lymphocytic leukemia.[37] Mechanistically, galectin‐9 has been reported to stabilize induced Tregs (iTregs) through binding to its receptor CD44.[38] Yang and colleagues reported that treatment with an antagonistic galectin‐9 monoclonal antibody in a syngeneic mouse colon carcinoma model led to the expansion of tumor‐infiltrating cytotoxic CD8+ T cells as well as Tregs. Here, HAVCR2 is linked to B-cell chronic lymphocytic leukemia.