Because Th17/IL-17 activity has been linked to inflammation, autoimmunity, and tumorigenesis [78,79,80], these results verify that p53 inactivation in immune cells augments inflammation-induced tumorigenesis via multiple pathways, such as enhancing production of inflammatory cytokines and chemokines, promoting the differentiation and function of Th17 cells, and suppressing the differentiation of Treg. The gene discussed is TP53; the disease is Autoimmunity.