As argued by the authors, in the absence of any effect of the same treatment protocol on subventricular zone neurogenesis in unchallenged mice, the positive effect of low dose C3aR antagonist treatment on post-stroke neurogenesis is conceivably due to the inhibition of the inflammation including the reduced recruitment of activated T-lymphocytes rather than to the direct effect of the drug on the progenitor cells [69]. This evidence concerns the gene C3AR1 and Stroke.