Additionally, in both in vivo and in vitro models of glioma, the mechanism by which dihydroartemisinin exerts anticancer effects on glioma cells was found to be dependent on promoting ferroptosis via the PERK–ATF4–heat shock protein family A member 5 (HSPA5)–GPX4 pathway (84). This evidence concerns the gene EIF2AK3 and central nervous system cancer.