Recent results in chronic viral infection and cancer have shown that strategies targeting dimeric intermediate-affinity IL-2Rs are inadequate for inducing antiviral and antitumor efficacy, and when trimeric high-affinity IL-2Rs are targeted, therapeutic efficacy combined with PD-1 blockade is effectively induced48,49,52 (Fig. 3a, b). The gene discussed is PDCD1; the disease is cancer.