Given that AHR activation in lung epithelia is associated with an enhanced CD4+ T-cell immune response [53, 54], it is plausible that its observed gradual inactivation in dysplasia, LCIS, and LSCC may lead to an altered immune response which facilitates oncogenesis, although the relation between AHR and inflammatory pathways is also complex and strongly model dependent [54]. This evidence concerns the gene CD4 and dysplasia.