CD86 and acute myeloid leukemia: Many of these regulatory mechanisms seem to be shared by solid tumors and hematology neoplasms including over-expression of inhibitory check-point receptors on T cells and their ligands on AML cells or DCs such as PD-1/PD-L1, CTLA-4/CD80/CD86, Tim-3/galectine-9 (gal-9), and Lag-3/MHCII, enzymes as IDO and induction of immunoregulatory populations expansion as Tregs (83–85).