There have been several reports suggesting that morphological changes and proliferation are dissociated in reactive astrocytes. First, injury-induced astrogliosis in GFAP/vimentin-deficient mice exhibits astrocyte proliferation comparable to that in wild-type mice . Moreover, spontaneous astrogliosis in mice deficient in FGFRs does not result in proliferation of reactive astrocytes . Immunogenic capacity is also likely dissociated from the proliferation and hypertrophy in reactive astrocytes, as spontaneous astrogliosis in mice deficient in Bax does not recruit reactive microglia . Nevertheless, the dissociated regulation of aspects of astrocyte reactivity is not clearly understood. The discrepancies between results obtained from Mlc1-ErbB2V664E and Mlc1-dnEGFR mice indicated that the proliferation of reactive astrocytes was regulated by signaling downstream of the initial reactive responses induced by ErbB activation and that it could be independent of ErbB receptor activation in astrocytes.