Günther and coworkers reported that TBE patients with encephalitis had significantly lower levels of IL-10, a potent anti-inflammatory cytokine, in CSF (days 7–18 of the clinical course of illness) than TBE patients with meningeal disease, but similar levels of IFNγ, IFNα, and IL-6, implying that the lower levels of IL-10 are not able to sufficiently control inflammatory responses in CSF, thereby contributing to pathophysiology of TBE [35]. The gene discussed is IFNG; the disease is tick-borne encephalitis.