Recently, it has been hypothesized that in patients with IPF an excessive recruitment of CD8+ TLs may occur in response to repeated viral infections and this excessive response may play a role in the development of lung damage through multiple mechanisms (nuclear factor κB, tumor necrosis factor α) of epithelial cells activation, production of chemokines by the alveolar cells which may in turn amplify inflammatory responses in the lung [28]. The gene discussed is CD8A; the disease is viral infectious disease.