To this end, the strategy of combination therapy of oncolytic E1B-deleted adenovirus with adenoviral vector encoding angiogenic inhibitors is more desirable in clinical settings, as cancer cells with nonfunctional p53 would be more susceptible to Ad5WS1-induced cytolysis than those with wild-type p53, while tumours retaining functional p53 more responsive to antiangiogenic therapy because of more vascular dependence. The gene discussed is TP53; the disease is cancer.