The binding of the receptor tyrosine kinase, c‐kit, to its ligand, stem cell factor (SCF), mediates numerous biological functions. Important roles for c‐kit in hematopoiesis, melanogenesis, erythropoiesis, spermatogenesis, and carcinogenesis are well documented. Similarly, activation of granulocytes, mast cells, and of eosinophils in particular, by c‐kit ligation has long been known to result in degranulation with concomitant release of pro‐inflammatory mediators, including cytokines. However, recent work from a number of laboratories, including our own, highlights previously unappreciated functions for c‐kit in immunologic processes. These novel findings strongly suggest that signaling through the c‐kit–SCF axis could have a significant impact on the pathogenesis of diseases associated with an immunologic component. In our own studies, c‐kit upregulation on dendritic cells via T helper (Th)2‐ and Th17‐inducing stimuli led to c‐kit activation and immune skewing toward these T helper subsets and away from Th1 responses. Others have shown that dendritic cell treatment with inhibitors of c‐kit activation, such as imatinib mesylate (Gleevec), favored breaking of T‐cell tolerance, skewing of responses toward production of Th1 cytokines, and activation of natural killer cells. These data all indicate that deeper understanding of, and ability to control, the c‐kit–SCF axis could lead to improved treatment modalities aimed at redirecting unwanted and/or deleterious immune responses in a wide variety of conditions.