No matter how heterogeneous astrocytes in different brain regions are , cell-autonomous ErbB activation in astrocytes induced similar reactive responses throughout the brain (Figure 4 and Supplementary Figures S7–S9). Intriguingly, prevalent astrogliosis and associated brain inflammation predominantly caused anorexia in animals (Figure 5). The susceptibility of different brain regions to reactive astrogliosis warrants further investigation. Nevertheless, the functional roles of astrogliosis in pathological development are still debated. For example, glial scar formation over injury sites has been shown to restrain damage but perturb axon regrowth in the CNS [72, 73]. However, a recent study reported astrocytic scars to be beneficial for axon regeneration . This paradox was solved by a more recent work that disrupting the molecular signaling specifically transforming reactive astrocytes into scar-forming astrocytes leads to enhanced axon regrowth, indicating a functional dissociation of different types of astrocytes that are sequentially induced during the development of reactive astrogliosis . Moreover, the type of CNS insult influences the outcome of astrogliosis in a context-dependent manner [5, 7]. Therefore, signaling pathways regulating astrocyte reactivity must be assessed in specific contexts to comprehensively evaluate the targets that contribute to or inhibit astrogliosis. It would be intriguing to determine whether ErbB inhibition alters functions other than scar formation in reactive astrocytes and whether these functions are required for specific pathological processes. Our work shed light on the molecular mechanisms that regulate astrocyte reactivity and described inducible animal models that could be useful for future investigations into the function of astrogliosis and potential therapeutic targets.