Moreover, the accumulation of ΔN-Bcl-xL is associated with mitochondrial injury or neuronal injury in both in vitro and in vivo models of cerebral ischemia [39,42,43,44]: glutamate-mediated excitotoxicity and ischemic strokes enhance the formation of endogenous ΔN-Bcl-xL in hippocampal neurons, promoting neuronal death [31,43]. Here, BCL2L1 is linked to ischemic stroke.