Adult neurogenesis in mammals is generally confined to specific regions where astrocytic cells produce particular neuronal types throughout life. Outside these areas, the capacity for neurogenesis is limited. However, on p. 840, Paolo Peretto, Federico Luzzati and co-workers provide evidence that striatal astrocytes can be activated to a neurogenic program in an adult mouse model of Huntington's disease. Following treatment with the toxin quinolinic acid to induce a lesion, the authors observe the appearance of proliferating progenitors and neuroblasts. Fate-mapping experiments identify local striatal astrocytes as the source of this neurogenic program. Importantly, neurogenesis is only observed upon lesion, suggesting that these astrocytes are normally quiescent but possess latent neurogenic potential upon damage. Further analysis is required to understand the programs regulating this neurogenesis, to determine the final fate of the newly born neuroblasts and to assess whether a similar phenomenon might exist in humans. However, these data open the possibility of harnessing the neurogenic potential of striatal astrocytes for therapeutic purposes.