After stroke, NSCs become activated and proliferate to expand the progenitor pool in the SVZ.2 The chemokine SDF1 (stromal cell-derived factor 1) is secreted by astrocytes and endothelial cells in the ischemic lesion, causing neuroblasts to divert from the rostral migratory stream (RMS) and instead migrate toward the lesion.3,4 Once there, they give rise to a limited number of neurons5 and secrete trophic factors.6 Ultimately, NSC migration toward the lesion is considered protective because genetic ablation of neural progenitors increases lesion sizes after stroke.5-7. Here, CXCL12 is linked to stroke disorder.