However, during inflammation-driven fibrosis, as observed in allergic asthma, pericytes have been observed to uncouple from capillaries within the airway wall and accumulate within and around airway smooth muscle bundles, with elevated expression of the myofibroblast marker α-smooth muscle actin (α-SMA) and a demonstrable contribution to airway hyperactivity in an allergen-driven model of allergic asthma (5). This evidence concerns the gene ACTA1 and allergic asthma.