This hypothesis is supported by several factors: (i) distinct gene expression profiles observed in rhinitis, which show a preference for toll-like receptor and IL-17 expression, as opposed to A + R, where IL-33 and IL-5 are more prominently expressed [10]; (ii) differing allergen sensitization patterns, with rhinitis typically involving mono- or pauci-sensitization, while A + R tends to show polysensitization [11,12]; (iii) the greater symptom severity observed in epidemiological studies [13,14]; (iv) real-life studies; and (v) differences in treatment response. This evidence concerns the gene IL33 and rhinitis.