Hedgehog (Hh) signaling is essential for development of all vertebrates and drives proliferation, migration, and differentiation of progenitor cells to pattern organ development. In vertebrates, Hh signals through an organelle called the primary cilium. Cilia are polarized microtubule-based signaling projections that nucleate from the centrosome-derived basal body and are found on almost every vertebrate cell, including epithelial and mesenchymal cells that make up the skin and hair follicle. Hh pathway activation begins when Hh ligand binds to and inhibits the transmembrane receptor Ptch1, allowing the signal transducer Smo to activate Gli transcription factors and amplify Hh target gene expression. Although the main players have been identified, how Hh pathway components work together and how they are regulated remains unclear. My colleagues and I have found that Missing-in-Metastasis (MIM), a multi-domain scaffold protein that links membrane dynamics with the actin cytoskeleton, regulates primary cilia formation and Hh responsiveness at the basal body to promote de novo hair follicle formation. MIM functions in part by inhibiting the activity of the oncogenes Src kinase and Cortactin to prevent actin polymerization at the base of the cilium. MIM also interacts with the oncogenic kinase aPKC to facilitate Hh signaling and ciliogenesis in hair follicles and basal cell carcinoma. How MIM mediates its effects on kinases remains poorly understood and we are currently identifying new interaction partners through tandem-affinity proteomic screens to gain insight into the underlying mechanism of scaffold-kinase regulation.