Utilizing this airway mycosis-dependent model of chronic eosinophilic sinusitis and allergic asthma, we previously demonstrated that STAT6-deficient mice and an intranasally applied small peptide inhibitor of STAT6 not only ameliorate pulmonary inflammation and airway hyperreactivity, but also now show that it essentially abrogated sinus inflammation and the influx of inflammatory effector cells to the sinonasal mucosa (10). The gene discussed is STAT6; the disease is allergic asthma.