We found that the slow tumor growth kinetic resulting from B7-H3 inhibition is markedly dependent on the presence of host IFN-γ and activation of the IFN-γ:IFNGR1 pathway in tumor cells (Fig. 6g, n): while knockdown of B7-H3 decreased Tsc2-deficient tumor growth by ~90% in wild-type mice, it had little effect in IFN-γ knockout mice or when IFNGR1 expression is knocked down in the tumor cells. The gene discussed is IFNGR1; the disease is neoplasm.