Targeting OGT or reducing O-GlcNAcylation in cancer cells leads to metabolic stress and ER stress response, including protein kinase R (PKR)-like endoplasmic reticulum kinase (PERK) activation, increased phosphorylated eukaryotic translation initiation factor 2 alpha (p-eIF2α) and CCAAT/Enhancer-binding protein homologous protein (CHOP) levels and apoptosis [47]. This evidence concerns the gene DDIT3 and cancer.