<s>[INST] context: Apoptosis results from the activation of enzymes called caspases (so named because they are cysteine proteases that cleave proteins after aspaic residues). The activation of caspases depends on a finely tuned balance between production of pro- and anti-apoptotic proteins. Two distinct pathways converge on caspase activation: the mitochondrial pathway and the death receptor pathway pro-apoptotic members of the family called Bax and Bak, which dimerize, inse into the mito- chondrial membrane, and form channels through which cytochrome c and other mitochondrial proteins escape into the cytosol. These sensors also inhibit the anti-apoptotic molecules Bcl-2 and Bcl-xL (see fuher on), enhancing the leakage of mitochondrial proteins. Cytochrome c, together with some cofactors, activates caspase-9. Other proteins that leak out of mitochondria block the activities of caspase antagonists that function as physiologic inhibitors of apop- tosis. The net result is the activation of the caspase cascade, ultimately leading to nuclear fragmentation. Conversely, if cells are exposed to growth factors and other survival signals, they synthesize anti-apoptotic members of the Bcl-2 family, the two main ones of which are Bcl-2 itself and Bcl-xL. These proteins antagonize Bax and Bak, and thus limit the escape of the mitochondrial pro-apoptotic proteins. Cells deprived of growth factors not only activate the pro-apoptotic Bax and Bak but also show reduced levels of Bcl-2 and Bcl-xL, thus fuher tilting the balance toward death. ref Robbins 9/e p19 [/INST] question: Which of the following is an antiapoptotic gene? | options: A: BAX B: BAD C: BCL-X D: BIM | answer: C </s>