Regarding allergic rhinitis (AR), both Okano et al. [63] and Baumann et al. [64] found that allergen-stimulated PBMCs produce IL-31 and correlate to the severity of the disease and its symptomatic manifestations, thus suggesting that IL-31 may increase inflammation in the nasal epithelium through the release of mediators (CCL17, CCL22, and CCL1), which recruit inflammatory cells, as seen in AD. The gene discussed is CCL17; the disease is allergic rhinitis.