Metabolic switching can therefore be exploited to target cancer cells using agents such as 2-deoxyglucose (2-DG), which interestingly as well as inhibiting glycolysis induces downregulation of MCL-1 levels with no change to BAK expression, suggesting that BAK activation would be increased in the absence of a key anti-apoptotic protein that binds and restrains its activation. This evidence concerns the gene BAK1 and cancer.