We found that PLP2 knockdown reduces cell proliferation and increases ER stress‐induced apoptosis and autophagy via CCAAT‐enhancer‐binding protein homologous protein (CHOP), a ubiquitous transcription factor known to have a regulatory role in the crosstalk between autophagy and apoptosis.20 Our results therefore establish a vital role for PLP2 in promoting GBM growth and as a potential therapeutic target. Here, PLP2 is linked to glioblastoma.