It has been hypothesised that airway epithelial loss of E-cadherin is a critical step in asthma pathogenesis [32]; supportive of this, siRNA silencing of E-cadherin resulted in reduced epithelial resistance in bronchial epithelial cells and led to increased expression of TSLP and C–C motif chemokine ligand 17 [22, 33]. This evidence concerns the gene CDH1 and asthma.