This may be explained by inflammatory mediators produced largely in the process of GERD, exemplified as IL-6 and IL-8,[54,55] which may induce repeated immune activation; other possible explanations may be the increasing antibody level caused by the reactivation of latent virus, or EBV reaction due to the weakened immune system of GERD patients, or even the increased vulnerability of GERD-effected individuals to EBV. The gene discussed is CXCL8; the disease is gastroesophageal reflux disease.