Additionally, we provide a systems immunology overview of immune subset interactions between T cells of different specificities and suggest that the exhaustion of anti-MAA T cells could be caused by interactions with Tregs, especially via Galectin9 and TIM3, and with tumor cells via PVR and TIGIT, poising a potentially interesting strategy to invigorate anti-MAA and tumor cell interactions with anti-TIGIT and anti-MAA and immune cell interactions with anti-TIM3 antibodies, which are both currently tested in phase III trials in various solid and hematological cancers47,48. The gene discussed is NAA10; the disease is neoplasm.