Eosinophilic inflammation is a hallmark of asthma, and exposure to Baltimore PM was a potent stimulus for an influx of eosinophils (as well as neutrophils) into the murine lung (Figures 1B, 2, 4) and synergistically induced eosinophil infiltration in asthmatic mice, likely major contributors to the sustained AHR response in PM-stimulated OVA-sensitized mice. The gene discussed is AHR; the disease is asthma.