Based on this assumption and according to significant increase of TIM-3 in CD8+ T-cells, it seems that remarkable over-expression of TIM-3 could compensate for lower Galectin-9 expression within the Galectin-9/TIM-3 pathway and this pathway could be a candidate pathway for ICB in B-ALL. The gene discussed is HAVCR2; the disease is precursor B-cell acute lymphoblastic leukemia.