Still more, NF-κB has been reported to perform a dual role in cerebral ischemia, which shows that hypoxia-ischemia induced two peaks of cerebral NF-κB activity: an early NF-κB activation contributing to neuronal damage by down-regulating Bcl-2 and Bcl-xL expression and a late NF-κB activation producing a neuronal protection by increasing Bcl-2 and Bcl-xL expression [12]. The gene discussed is BCL2L1; the disease is brain ischemia.