In the central nervous system (CNS), specialised cells called oligodendrocytes produce the myelin sheath that insulates axons and enables fast nervous conduction. As seen in multiple sclerosis, myelination defects can lead to severe neurological problems. Now, Colognato, Müller and colleagues report findings that support the disputed notion that the extracellular matrix receptor β1 integrin is crucial for CNS myelination(see p. 2717). They report that in two mouse mutants in which β1 integrin was conditionally ablated in the CNS, CNS myelination defects were present that were not due to aberrant oligodendrocyte differentiation or survival. Instead, their in vitro experiments show that β1 integrins regulate myelin sheet outgrowth by activating the serine/threonine kinase AKT, and that constitutively active AKT can rescue the outgrowth defects caused by β1 integrin loss. Together these findings reveal that β1 integrin promotes the myelin wrapping of CNS axons in an AKT-dependent manner, opening the door to future studies into the downstream effectors of AKT and their role in myelination.