Considering that the TIM-3 function is linked to T-cell exhaustion and dysfunction in the anti-tumor immunity of cancer patients and TIM3 is usually increased in both the peripheral blood and bone marrow of patients with T-ALL [29, 41, 42], we think that the mechanism and effect of targeting TOX/TOX2-TIM3 axis in anti-T-ALL therapy will be complex and limited. This evidence concerns the gene HAVCR2 and neoplasm.