Finally, although Tax expression in HTLV-1-infected individuals is tightly regulated and often silenced to evade immune detection, especially in ATLL patients, it can still be reactivated by multiple stressors, such as hypoxia, T-cell reactivation and oxidative stress, thereby sustaining viral persistence and long-lasting proinflammatory immune responses (42–44). The gene discussed is CNTN2; the disease is adult T-cell leukemia/lymphoma.