Numerous studies have clearly shown that the Th2 cytokine, interleukin (IL)-13, is the central regulator of the allergic diathesis. Initial studies in animal models of disease provided compelling evidence that IL-13, independent of other Th2 cytokines, was both necessary and sufficient to induce all features of allergic asthma. The importance of IL-13 in allergic disorders in humans is supported by consistent associations between tissue IL-13 levels and genetic variants in the IL-13 gene with asthma and related traits. With the preponderance of evidence continuing to support the importance of IL-13 in allergic disorders, attention is now turned toward understanding the mechanisms by which this cytokine might mediate the pathophysiologic features of allergic disease. The emerging paradigm is that IL-13 induces features of the allergic response via its actions on epithelial cells and smooth muscle cells, not through traditional effector pathways involving eosinophils and IgE-mediated events. In light of these recent developments, in this review our current understanding of the role of IL-13 in the pathogenesis of asthma is explored, with a particular focus on new insights into the mechanisms by which IL-13 induces the features of asthma.