Our data now point to a differential role in atherosclerosis, which can be explained by unique functions of IL-4 and IL-13 as a consequence of the exclusive engagement of the alternative receptors IL-4Rα/γc and IL-13Rα2, respectively, or by differences in ligand affinity for the same IL-4Rα/IL-13Rα1 receptor complex (Kelly-Welch et al, 2003; LaPorte et al, 2008). The gene discussed is IL4; the disease is atherosclerosis.