This is an important observation as it indicates that cellular stressors are occurring in OLP, probably linked to DNA damage associated with autoimmune aggression, which triggers the TP53 gene out of its "standby" state, activating post-translational mechanisms that increase p53 protein production and its stabilisation in the nucleus to exert its tumour suppressor functions (69). The gene discussed is TP53; the disease is oral lichen planus.