This restored the numbers of functional CD8+ T cells in the tumor, as well as synergized with checkpoint inhibitor therapies (anti-CTLA4 and anti-PD-1 antibodies; treatments which directly interfere with additional, direct pathways by which cancer cells “switch off” CD8+ T cells) to promote tumor regression in syngeneic mouse models [22]. Here, CTLA4 is linked to neoplasm.