Myelination is one of the last events during mammalian brain development and is thought to continue into young adulthood in humans. Even in adulthood, ongoing low-level myelination is essential for neural homeostasis, and for dynamic processes such as learning and memory. Deficits in myelination resulting in abnormal white matter and disruption of neuronal function are observed in a wide variety of disorders of the CNS. One strategy for alleviating these deficits is to enhance the genesis of myelin-forming oligodendrocytes from their upstream precursor parents, oligodendrocyte precursor cells (OPCs). However, the capability of these OPCs to contribute to remyelination in injury or disease in the adult CNS remains unclear. To better understand adult oligodendrogenesis and remyelination, our guests today characterized and compared murine OPCs during early postnatal myelination with those from adult injury-induced adult remyelination. Their findings identify two developing OPC groups subserving distinct postnatal functions and suggest that neonatal and adult OPC-mediated oligodendrogenesis are fundamentally different, The findings have important implications for therapeutic interventions aimed at myelin repair.