For example, TH1 cells, upon activation by ICB, secrete interferon-γ (IFN-γ) and then directly potentiate intercellular adhesion molecule (ICAM)−1 and drive T cell migration, thereby promoting tumor vascular normalization and regression via the IFN-γ receptor on cancer endothelial cells [36], ultimately inhibiting tumor growth, enhancing vessel perfusion, and decreasing intratumoral hypoxia [37]. This evidence concerns the gene IFNG and neoplasm.