Based on these data, we propose a model illustrated in Figure 8: upon hapten sensitization and challenge, T cells secrete IL-3, which binds to IL-3 receptor complex on basophils and induces expression of ALDH1A2, resulting in the production of RA by basophils; in turn, RA activates RAR/RXR receptor heterodimer in basophils in an autocrine manner, and thereby upregulates the expression of integrins ITGAM, ITGB2, ITGA2B, and ITGB7, promotes the interaction between basophils and ECs, and eventually permits basophil extravasation to ACD skin. The gene discussed is ITGB2; the disease is granular corneal dystrophy type II.