Airway smooth muscle cells (ASMCs) have more than a single “function.” In addition to an obvious contractile function that regulates rapid changes in airway caliber, these cells have both a proliferative function that leads to hyperplasia and hypertrophy of smooth muscle in persistent asthma, and a secretory function that contributes to the extracellular matrix and modulates airway inflammation by elaboration of cytokines, mediators, and growth factors (1–3). Now, an emerging new function for these cells is cell migration—a capability of ASMCs that may have importance during the airway remodeling of persistent asthma. In this issue of the AJRCMB, Goncharova and coworkers compare cultured human ASMC migration to vascular smooth muscle cell (VSMC) migration, and test the effects that asthma medications ( -adrenergic agonist, phosphodiesterase inhibitor, and glucocorticoids) have on migration stimulated by platelet-derived growth factor (PDGF) (4).