The inhibition of T-cell immunity and the production of IFN-γ and an increase in levels of vasoactive mediators—eicosanoids (LTB4, TXB2) and cytokines (TNF-α, IL-4)—were observed for asthma in clinical remission, indicating the persistence of the inflammatory process due to the activation of Th2-type immune response. The gene discussed is IL4; the disease is asthma.