Since apoA-I and apoA-IV have been shown to (i) suppress eosinophil effector function and (ii) eosinophilic diseases such as allergic rhinitis and asthma are linked to apolipoprotein dysregulation, these endogenous proteins or stable peptides derived from them may represent a promising target for the prevention and therapy of eosinophilic inflammation. This evidence concerns the gene APOA1 and allergic rhinitis.