We also characterized the increased proliferation of reactive astrocytes. Some of the reactive astrocytes induced by stab injury in both Mlc1-dnEGFR and control mice were immunopositive for the proliferation marker Ki67 (Figure 3a). In addition, reactive astrocytes were frequently labeled with Olig2 immunostaining (Figure 3b). The basic helix-loop-helix transcription factor Olig2 has recently been identified as a protein hallmark of astrogliosis , despite being a key factor in determining motor neuron and, subsequently, oligodendroglial fate in NSCs during embryonic development . In the normal brain, the majority of Olig2+ nuclei, which indicate oligodendroglial lineage, are distributed in the white matter, with only sparse localization of Olig2+ cells in the cerebral cortex. Notably, increased Olig2+ nuclei in the parenchyma have been discovered in stab-, freeze-, ischemia- or Aβ deposit-injured cerebral cortical tissues [33, 35, 36], with many localized in reactive astrocytes [33, 36]. Lineage tracing studies have demonstrated that Olig2+ astroglial cells are an essential source of increased reactive astrocytes in response to injury . Indeed, some Olig2+ nuclei were also positive for Ki67 in the stab-injured cortex (Supplementary Figure S6). Surprisingly, neither the proportion of Ki67+ nor that of Olig2+ reactive astrocytes were changed in Mlc1-dnEGFR mice (Figure 3c), suggesting that dnEGFR did not affect their proliferation.