Moreover, TGF‐β signaling in astrocytes has been also shown to be necessary for limiting neuroinflammation in a mouse experimental stroke model (Cekanaviciute et al., 2014), whereas treatment of rat primary astrocytes with TGF‐β1 could completely reverse the pro‐inflammatory astrocytic phenotype caused by IL‐1α, tumor necrosis factor alpha (TNF‐α) and complement component 1q (C1q) stimulation (Liddelow et al., 2017). The gene discussed is TGFB1; the disease is stroke disorder.