A range of stimuli involved in asthma pathogenesis, including respiratory viruses, proinflammatory (TNF-α and IL-1β) and T2 (IL-4 and IL-13) cytokines, and proteolytic allergens have been shown to cause increased expression and release of TSLP from airway epithelial cells through activation of different PRRs and cytokine receptors, supporting its function as an alarmin signaling a compromised airway epithelium [78,123,126,131,132,133,134]. This evidence concerns the gene TSLP and asthma.