AKT1 and Stroke: Bioinformatic analyses further revealed that miR‐98‐3p was a key component of hypoxic preconditioning, through which NSC‐EVs upregulated the activities of phosphoinositide‐3‐kinase (PI3K)/protein kinase B (AKT), mitogen‐activated protein kinase (MAPK), mammalian target of rapamycin (mTOR), and endocytosis signaling pathways to facilitate cell survival in a stroke therapy.161