ErbB receptors (ErbB1–4), another family of receptor tyrosine kinases, and their ligands, including epidermal growth factor (EGF), neuregulin (NRG) and transforming growth factor α (TGFα), have been reported to increase in tissues with reactive astrogliosis [19–21]. In the nervous system, ErbB receptors are differentially expressed across various neural cell types and regulate many developmental and pathological events [16, 17, 22]. Once ligand bound, ErbB receptors dimerize and activate multiple intracellular signaling pathways, including Akt/mechanistic target of rapamycin, Erk and STAT3, to potently regulate cell proliferation, survival, differentiation, migration and inflammatory responses [16, 17, 22]. Both mutations and post-transcriptional alteration of ErbB receptors have been implicated in neurological disorders, including demyelination, stroke, epilepsy and psychiatric disorders [16, 22]. However, it remains unknown whether aberrant ErbB signaling in astrocytes participates in disease progression.