Therefore, it is important for us to better define the following: (1) whether the level or duration of p53 activation dictates the immunological outcome of antitumor immunity so that unnecessary damages can be controlled or avoided altogether, and (2) whether the tumor/host p53 dysfunction, either pre-existing or therapy-induced, may skew antitumor immunity to pro-tumor inflammation. This evidence concerns the gene TP53 and neoplasm.