Remarkably, a previous study reported the synergistic combined effects of Se-Y and FO on apoptosis induction in A549 lung adenocarcinoma cells via AMP-activated protein kinase (AMPK) activation and the opposite regulation of proapoptotic CCAAT/enhancer-binding protein homologous protein (CHOP) and cytoprotective glucose-regulated protein 78 (GRP78) endoplasmic reticulum (ER) stress-response elements, accompanied by a decrease in β-catenin and cyclooxygenase-2 (COX-2) [16]. This evidence concerns the gene DDIT3 and lung adenocarcinoma.