IL13RA1 and asthma: Through a series of experiments with knockout models of IL-13 signaling, including knockout mice lacking IL-13Rα1 or IL-4Rα, Munitz et al, demonstrated that key pathogenic molecules associated with asthma severity, such as chitinase, are entirely dependent on IL-13 signaling through IL-13Rα1, a component of the type II receptor.