The EA subtype manifests as the secretion of Th2-type cytokines (IL-4, IL-5, IL-13) and the expression of type 2 innate lymphocytes (ILC2), downstream of which a Th2-type immune response occurs, and then IL-4 stimulates the expression of polyfilament proteins in bronchial epithelial cells, which are important genes for the development and progression of EA (Carr et al., 2018; Gao et al., 2021). Here, IL5 is linked to Esophageal atresia.