Moreover, IL-13 has a dual nature; it is implicated in tissue repair processes following lung injury (it aids in matrix remodeling and the induction of epithelial-derived type 2 effector molecules, which are crucial for effective repair and recovery from lung damage) [64], and it has been shown to impair the integrity of the bronchial epithelial barrier by disrupting tight junctions, which can exacerbate asthma symptoms and potentially contribute to ALI. This evidence concerns the gene IL13 and asthma.