By mechanisms which remain to be fully elucidated, a disrupted epithelial structure can be the first step towards the development of asthma and CRSwNP resulting in an alarmin response (TSLP, IL-25, and IL-33) disproportionate to the inhaled triggers, which can further exacerbate the disruption of the airway epithelium [63]. This evidence concerns the gene TSLP and asthma.