Interestingly, both Bcl-2 and Bax expression levels were up-regulated in ATF4-proficient cells, compared with the control cell lines, while the expression of Bax showed only slight changes, indicating that an up-regulation of the Bcl-2 to Bax ratio might suppress the drug-induced apoptosis in ATF4-overexpressing gastric cancer cells. Here, BCL2 is linked to gastric cancer.