Many molecular signals released from various cell types are involved in regulating astrocyte proliferation after CNS injury. For example, FGF, Sonic hedgehog, endothelin-1 and STAT3 signaling pathways promote the proliferation of reactive astrocytes [18, 67–69]. Intriguingly, inhibiting inflammation abolishes both Sonic hedgehog activation and proliferation of reactive astrocytes in injured brains . STAT3 can be activated by FGFRs, ErbB receptors and cytokine receptors [57, 70, 71]. Note that reactive astrogliosis is usually complicated by interactions among reactive astrocytes, microglia, endothelial cells and other cell types . We found that although reactive astrocytes caused by cell-autonomous ErbB activation induced local inflammation (Supplementary Figure S9), immunogenic stimuli released from non-astrocytes could not be blocked by ErbB inhibition in astrocytes. In fact, the number of reactive microglia (Iba1+ cells) and cytokine mRNA levels were not reduced in injured cortices of Mlc1-dnEGFR mice (Figure 8a–c). Moreover, STAT3 activity (pSTAT3) was not reduced in either injured cortical tissues or CNTF-treated primary astrocytes from Mlc1-dnEGFR mice (Figures 7 and 8). These results suggest that some aspects of astrogliosis, including proliferation, are regulated by many coordinated signaling pathways that are stimulated by reactive astrocytes themselves or by other sources (Figure 8h, working model). Among them, the mechanism by which ErbB receptors and FGFRs antagonize each other in reactive astrocytes and cross-talk with STAT3 pathways through inflammatory signals deserves further investigation.