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. Here, CCL1 is linked to allergic rhinitis.