[27], [29] Gal-9′s attenuation of such disorders in mast cells [29] was due to suppression of degranulation, rather than induction of cytokines and chemokines, probably independent of TIM-3, since TIM-3-deficient mice normally developed allergic airway inflammation. [28] However, treatment with Gal-9 after antigen challenge may exacerbate inflammation in the late phase of allergic diseases by enhancing cytokine and chemokine production by mast cells and recruiting eosinophils to local inflammatory sites. This evidence concerns the gene HAVCR2 and allergic disease.