Yuan et al. verified that the deletion of CCR3 reduced eosinophilic inflammation and the Th2 immune response by inhibiting the PI3K-AKT pathway in allergic rhinitis mice, and targeted knockout of CCR3 inhibited the expression of the PI3K-AKT signaling pathway in eosinophils and the proliferation, migration, and degranulation of eosinophils in vitro experiments [43]. The gene discussed is AKT1; the disease is allergic rhinitis.