Silencing of RGC‐32 expression abolishes C5b‐9‐induced proliferation of human aortic endothelial cells in vitro.15 Reportedly, RGC‐32 expression is also involved in TGF‐β1‐induced ECM production from astrocytes of experimental autoimmune encephalomyelitis (EAE) mice.44 However, the expression and role of RGC‐32 in the GMC proliferative response triggered by sublytic C5b‐9 in rat Thy‐1N remains unclear. This evidence concerns the gene TGFB1 and experimental autoimmune encephalomyelitis.