Exposure to DiNP has been associated with the aggravation of airway remodelling and airway hyperresponsiveness (AhR) in individuals progressing from atopic dermatitis (AD) to asthma. It induces an increase in interleukin-33 (IL-33), immunoglobulin E (IgE), Th2 and Th17 cytokines, and the expression of thymic stromal lymphopoietin (TSLP). The gene discussed is IL33; the disease is asthma.