Considering that in the absence of FGL2, DCs in the spleens of ID8-p53−/−Brca2−/− tumour-bearing mice were more activated, but were excluded from the tumour, we therefore combined immunotherapeutic strategies in order to convert the “cold” tumour (MHC-I low54, excluded activated DC) into a “hot” tumour55,56. The gene discussed is TP53; the disease is neoplasm.