Additionally, compounds present in tobacco smoke have been shown to facilitate epicutaneous sensitization by promoting Langerhans cell migration, inducing the release of epithelial alarmins such as TSLP (Thymic stromal lymphopoietin) and IL-33, and enhancing Th2- and Th17-skewed immune responses, suggesting a plausible mechanism through which ETS exposure may contribute to the development of atopic eczema [85,86]. This evidence concerns the gene IL33 and atopic eczema.