This poor immunogenic response has been proposed to be related to the low mutational burden in ALL [2], qualitative or quantitative defects in HLA expression [14], and an imbalance in the expression of co-stimulatory or inhibitory molecules (PD-1/PDL-1 pathway, CTLA-4, or TIM-3) [15,16,17]. Here, HAVCR2 is linked to acute lymphoblastic leukemia.