It also inhibits Mcl-1 expression in glioma cells in a dose-dependent manner, by proteasomal degradation; thus, it sensitizes tumor cells to favor the effect of ATB-737, causing the loss of mitochondrial membrane potential and inducing apoptosis, as demonstrated by the cleavage of caspase-3 and PARP, cyt c, and Smac/DIABLO cytosolic accumulation, as well as Bax activation [301]. Here, MCL1 is linked to central nervous system cancer.