In chickens infected with Rous sarcoma virus, a known oncogenic virus, inflammation appears to be responsible for sarcoma induction at the site of experimentally inflicted wounds, possibly mediated by TGF-β and other factors, and released by inflammatory cells at the site of injury [211–220]; TGF-β is a major mediator of fibrosis and may promote tumor development through immunosuppression and the initiation of angiogenesis, possibly through signalling involving the Smad pathway [221–224]; mice lacking Smad3 show accelerated wound healing and a reduced local inflammatory response [225, 226]. This evidence concerns the gene TGFB1 and neoplasm.