The c-kit receptor tyrosine kinase’s (c-kit) binding to its ligand, stem cell factor (SCF), promotes a variety of biological actions. c-kit has critical functions in hematopoiesis, melanogenesis, erythropoiesis, spermatogenesis, and carcinogenesis. Similarly, c-kit ligation has long been known to cause degranulation of mast cells and eosinophils, as well as the production of pro-inflammatory mediators such as cytokines. This review will focus on a recently found c-kit function in modulating adaptive immune responses that is relevant to allergy disorders. For this research, a variety of laboratories has revealed hitherto unknown activities for c-kit in immunological processes. Increased expression of c-kit and its ligand, SCF, on dendritic cells in response to Th2/Th17-inducing stimuli results in c-kit activation and immunological skewing toward these subsets rather than Th1. Treatment of dendritic cells with c-kit activation inhibitors, such as imatinib mesylate, results in a breach of T-cell tolerance, a shift toward Th1, and the activation of natural killer cells. These findings imply that the c-kit/SCF axis might be a potential target for diverting harmful immune responses in a variety of illness situations, including allergy disorders, which are frequently linked with Th2 and Th17 responses.