Accumulating evidence has indicated that an increase in the Bcl-2 (Bcl-xL)/Bax ratio inhibits Bax translocation to the mitochondria and protects neurons against apoptotic insults, whereas a shift in the balance toward an excess of Bax elicits ischemia-induced neuronal apoptosis [16,49,50]. The gene discussed is BCL2L1; the disease is ischemia.