Subsequently, we have demonstrated a role of proinflammatory (IFNγ, IL1β, TNFα, and IL6) and anti-inflammatory (IL4, IL10, and TGFβ) cytokines, in our GBS cohort [17] and in an experimental animal model [20], and concluded that Th1 cytokines in the early disease course were associated with immune-mediated disease progression due to neuronal inflammation, but Th2 immune response during the later phase helped in recovery from the disease. The gene discussed is IL1B; the disease is Guillain-Barre syndrome.