Given that Fgl2−/− DCs have more co-stimulatory molecules, we expected that the absence of FGL2 would correspond to more T cell activation and therefore we characterized tumour-infiltrating T cells and splenic T cells in B16F10 or ID8-p53−/−Brca2−/− tumours implanted into Fgl2WT and Fgl2−/− mice. The gene discussed is TP53; the disease is neoplasm.