The apparent contradiction that activation of both TRPV1 and TRPA1 causes neurogenic airway inflammation, but only TRPA1 agonists produce hallmark features of airway inflammation in models of asthma and COPD [20], [22], [25], could be explained if TRPA1 channels were expressed not only by sensory nerves, but also by non-neuronal cells of the airways, from which they orchestrate neurogenic-independent inflammatory responses. The gene discussed is TRPA1; the disease is asthma.