Class 3 secreted semaphorin (Sema3A) is a chemorepellent that acts upon a wide variety of axons. As such, it induces a dramatic redistribution and depolymerization of actin filaments that results in growth cone collapse. Plexins are single membrane-spanning signaling proteins encompassing Plexin A1, A2, A3, and A4. Plexins form a complex with neuropilin-1 and -2 and the cell adhesion protein L1 to form a functional semaphorin receptor (1,2). The GTPase Rnd1 binds to the cytoplasmic domain of Plexin A1 to trigger cytoskeletal collapse. In contrast, the GTPase RhoD blocks Rnd1-mediated Plexin A1 activation and repulsion of sympathetic axons by Sema3A (3). Sema6A is also a ligand for Plexin A2. Both Sema6A and Plexin A2 knock-out mice have a granule cell migration defect, where cells remain in the molecular layer. Furthermore, Plexin A2 also controls nucleus–centrosome coupling which modulates cell migration (4).