According to earlier research, the CLL cells upregulate the expression of Gal-9 and PD-L1 in order to engage with the inhibitory receptors Tim-3 and PD-1, resulting in induction of exhaustion processes in infiltrating CD8 + T cells and escape of immune effector anti-tumor mechanisms [17]. This evidence concerns the gene HAVCR2 and B-cell chronic lymphocytic leukemia.