AdV infection (also possibly by alternative virus entry) with a low virus burden on IL-10 secretion allows the production of other pro-inflammatory cytokines and increases CD8+ T cell cytotoxicity, while an extremely high AdV vector burden in the tumor microenvironment suppresses IL-10 production and does not limit the intensity and duration of the local immune response [13,89]. This evidence concerns the gene CD8A and neoplasm.