There is increasing evidence that TIM3 expression is elevated in CML stem cells, CD4+ and CD8+ T cells in both primary and relapsed patients with chronic myeloid leukemia (CML), inducing T-cell depletion, and that blocking TIM3 may improve the immune response generated by the discontinuation of TKI inhibitors and concurrently target leukemic stem cells, preventing the disease from relapsing (38, 39). Here, HAVCR2 is linked to chronic myelogenous leukemia, BCR-ABL1 positive.