Moreover, since delayed anti-PD-1 treatment was ineffective in suppressing tumor growth in more than half of the anti-4-1BB-pretreated mice (Fig. 6i), we conclude that the enhancement of antitumor CD8+ T cell proliferation and the development of granuloma in TDLNs as a feedback inhibitor of the excessively enhanced CD8+ T cell responses are two sides of the same coin in controlling overall antitumor immunity. The gene discussed is CD8A; the disease is neoplasm.