Accumulating evidence has indicated that an increased ratio of Bcl-2(Bcl-xL)/Bax prevents the activation and translocation of Bax to the mitochondria, leading to antiapoptosis, whereas a decreased Bcl-2(Bcl-xL)/Bax ratio induces mitochondrial Bax homo-oligomerization, leading to the formation of pores in the mitochondrial outer membrane, and subsequent activation of the cytochrome c-mediated apoptotic cascade in the ischemic area after cerebral ischemia [16–18]. This evidence concerns the gene BCL2L1 and brain ischemia.