Programmed cell death, or apoptosis, is a critical failsafe against uncontrolled proliferation. For this reason, apoptosis is frequently defective in cancer cells, allowing tumor growth to proceed unchecked. The inhibitor of apoptosis proteins, or IAPs, are some of the final “brakes” on apoptosis, directly inhibiting both caspases and their upstream activators (1,2,3,4). Thus it is unsurprising that IAP proteins are over-expressed in many human cancers (2,5).