Therapeutic efforts to boost anti-tumor CD8+ T cell immunity have focused on manipulating several aspects of CTL function including re-activation of exhausted CTLs (anti-PD1, LAG3 and TIM3 monoclonal antibodies) [6], expansion of highly reactive tumor infiltrating T cells (Adoptive Cell Transfer Immunotherapy) [13], boosting tumor antigen specific T cell responses (cancer vaccines employing neoantigens and tumor associated antigens) [14] and boosting CTL priming (CD27 agonists) [15]. The gene discussed is HAVCR2; the disease is neoplasm.