A small-molecule inhibitor, PNRI-299, that targeting the oxidoreductase redox effector factor-1, selectively inhibits AP-1 transcription, without affecting NF-κB transcription, significantly reduces airway eosinophil infiltration, mucus hypersecretion, edema, and lung IL-4 levels in a mouse asthma model [110]. This evidence concerns the gene JUN and asthma.