For example, insulin has been proven to inhibit the expression of asthma-related genes (such as IL-4, ADAM-33, and LIGHT), thereby possibly reducing the inflammatory response.[22] Furthermore, Insulin resistance-related hyperinsulinemia is linked to α-smooth muscle actin and peribronchial collagen deposition, and higher β-catenin levels. This evidence concerns the gene IL4 and hyperinsulinism.