Another study investigating the anti‐ER stress mechanisms of gamma‐tocotrienol using +SA mammary tumor epithelial cells have reported that its mode of action in producing anti‐apoptotic effects is not by mitochondrial dysfunction or the death receptors but by increasing PARP cleavage and activation‐mediated protein kinase‐like ER kinase/eukaryotic translational initiation factor/activating transcription factor 4 (PERK/eIF2alpha/ATF‐4) pathway, which is a marker of ER stress response.178. This evidence concerns the gene ATF4 and breast cancer.