More importantly, Tregs at a tumor site overexpress inhibitory receptors CTLA-4, PD-1, TIM-3, and LAG-3 and up-regulate expression of TGF-β-associated LAP and GARP molecules and NRP-1 (32, 74), further enhancing their capability to suppress antitumor functions and, thus, contributing to tumor escape from the host immune system. The gene discussed is HAVCR2; the disease is neoplasm.