To investigate whether ErbB signaling is required for reactive astrogliosis, we used an acute brain injury model in which the parietal cortices of mice, aged postnatal day 30 (P30), were exposed and injured via a needle puncture. Three to 21 days later, brains were isolated, sectioned and immunostained for GFAP. Increased GFAP expression is a clear hallmark indicating the transition of normal astrocytes to reactive astrocytes [5–7]. Both Mlc1-dnEGFR and littermate control mice exhibited increased GFAP+ cells adjacent to the injury sites, with comparable distributions (Supplementary Figure S3a). Reactive astrocytes possess a molecular profile distinct from that of normal astrocytes [5, 7, 28]. For example, nestin, the protein marker for NSCs, appears to be a molecular hallmark of reactive astrocytes induced by various insults [29, 30], and it appeared in reactive astrocytes in either Mlc1-dnEGFR or control cortices 3 days after injury (Supplementary Figure S3b).