GFAP and stroke disorder: Although the activity of the GFAP promoter and thus of the C3a transgene is too low to affect the levels of basal hippocampal and subventricular zone neurogenesis in unchallenged adult GFAP-C3a mice [81], pronounced and persistent reactive gliosis in the peri-infarct tissue [82] results in sufficiently high transgene-derived C3a levels to impact post-stroke neurogenesis in this region.