Thus, these data provide an independent confirmation of the critical NR2F6 function in T cell-mediated cancer immunity, strongly suggesting that in combination with either of the approved PD-L1 and CTLA-4-targeted immune checkpoint therapies, T cell-based ACT therapies have increased efficacy from modulation of the NR2F6 inhibitory signaling pathway. The gene discussed is CTLA4; the disease is cancer.