Thus, it appears that patients with ME/CFS attempt to maintain a state of transient hypoglycemia caused by increased proinflammatory cytokines, hyperinsulinemia, and hypocortisolism to maintain a chronic innate immune response, decreased viral replication, and enhanced CD8 T-cell effector response [247–249], though without being able to resolve the infection by presenting an alteration in CD4 T cell function and, therefore, a deficient cytotoxic response of CD8 T cells in individuals with “weak” HLA-II haplotypes against EBV. The gene discussed is CD8A; the disease is hyperinsulinism.