The underlying mechanism proposed is that all-trans-retinoic acid (ATRA) accumulation in the lungs promotes asthma inflammation via activation of COX-2 expression and subsequent induction of prostaglandin pathway (PGD2 synthesis), including the synthesis of the Th2 cytokines IL4, IL5 and IL13 while decreasing IFNγ and, TNFα expression and IL12 synthesis in activated T-cells [146]. The gene discussed is IL5; the disease is asthma.