In previous studies of asthma, airway epithelial linking E-cadherin molecule is considered the “gatekeeper” of the airway mucosa [21], and when E-cadherin expression is disrupted it enhances signaling between epithelial cells and underlying immune and structural cells, which may lead to allergic sensitization and airway remodeling, including goblet cell hyperplasia, and smooth muscle cells conversion to a proliferative phenotype [68–70]. This evidence concerns the gene CDH1 and asthma.