In a study published in 2017, it was shown that patients with asthma had lower expression of GLP-1 receptor in eosinophils than healthy controls; additionally, the exposure of patients to GLP-1 analogs significantly decreased the expression of eosinophil surface activation markers after LPS stimulation and reduced eosinophil production of IL-4, IL-8, and IL-13, but not IL-5, which would be in favor of a paradoxical reaction [39]. The gene discussed is GLP1R; the disease is asthma.