Studies have shown that activating PERK/ATF4 promotes cholesterol efflux in hepatocytes by inhibiting the expression of high‐density lipoprotein (HDL) receptor, SR‐BI (scavenger receptor class B, type I)[48] and upregulating the transcription levels of ABCA1.[35] Thus, targeting the PERK/ATF4 signaling arm of ERS/UPR could be a potential therapeutic approach for glioma from the perspective of cholesterol metabolism. The gene discussed is ATF4; the disease is glioma.