These inflammation-associated, generally highly differentiated keratinized lesions commonly carry mutations in the tumor suppressor genes TP53 and CDKN2A. Missense TP53 mutations lead to accumulation of p53/agerrant p53 in the nuclei of proliferating tumor cells (nuclear overexpression), which serves as a surrogate marker for a TP53 missense mutation. The gene discussed is TP53; the disease is neoplasm.