BCL-2 family proteins (Bcl-2, Bcl-xL, Mcl-1, etc) are typically thought to prevent cell death by inhibiting the pro-apoptotic action of other BH3 family proteins.  This paper (as well as previous work from the Hardwick lab) demonstrates how an N-terminal fragment of Bcl-xL, presumably generated by caspase cleavage, can actually act as a lethal stimulus to kill neurons following ischemia.  The complex anti- and pro-death activities of Bcl-2 family members is fascinating.