Withaferin A also attenuated the development of glioblastoma multiforme (GBM), both in vitro and in vivo, by inducing endoplasmic reticulum stress via activating the transcription factor 4-ATF3-C/EBP homologous protein (ATF4-ATF3-CHOP) axis, which would be essential for optimizing withaferin A-based therapy to treat GBM by activating apoptosis and cell cycle inhibition at the G2/M level [103]. This evidence concerns the gene TCF4 and glioblastoma.