The activation of both types of IL-4 receptors leads to the phosphorylation of Janus kinase (JAK) 1, Jak2, and Tyk2, activating STAT-6 transcription factors and leading to the gene expression of target inflammatory mediators.19–21 Therefore, suppressing the IL-4/IL-13 axis presents an attractive therapeutic target in asthma. Here, STAT6 is linked to asthma.