Co-expression of CLC and PSG2, the two genes involved in the limitation of Th2- and induction of Th17-differentiation in EA patients, suggests both a counterweight mechanism to limit T2-response and a possible role behind the heterogeneity of T2-high asthma, recently proposed to be divided into IL-5-high/IL-17F-high asthma (with mixed granulocytic infiltration) and IL-4/IL-13-high asthma (with eosinophilic infiltration alone). This evidence concerns the gene CLC and Esophageal atresia.