AML cells can decrease MHC-I/II expression, produce reactive oxygen species (ROS) and indolamine-2,3-dioxygenase (IDO), and increase inhibitory ligands PDL1, B7-H3 (CD276), and Galectin 9 (Gal), which lead to escape immune surveillance and T cell exhaustion [12]. This evidence concerns the gene CD276 and acute myeloid leukemia.