During stroke induction, a significant population of nestin+ NPCs within the SVZ are diverted from their initial migration route toward the peri‐infarct region, signifying a possible role for them in poststroke recovery.[14] FOXO3 modulates the homeostasis of NPCs, to preserve cell quiescence and prevent premature differentiation, by inducing a program of self‐renewal genes.[15] Upregulation of FOXO3 induction by hypoxia‐ischemia[16] is linked to the hypothesis that activating FOXO3 expression using a specific therapeutic strategy can promote the proliferation of NPCs for recovery poststroke. The gene discussed is FOXO3; the disease is stroke disorder.