The Friesen Lab has resolved a twenty-year-long quandary in the field of viral apoptosis by explaining how viruses prevent apoptosis to gain a replicative advantage. Host cell apoptosis effectively stops intracellular parasites like viruses. Baculoviruses, a family of prolific insect DNA viruses, have therefore evolved strategies for preventing apoptosis. To this end, baculoviruses pirated the cellular inhibitor of apoptosis (IAP) protein to evolve the viral IAP. The viral IAP has optimized anti-apoptotic function, whereas the cellular IAP acts as a molecular switch to decide between life and death. Cellular IAPs, which are depleted to allow apoptosis, block pro-apoptotic proteins or pro-death proteases called caspases. The Friesen lab recently discovered the unique strategy by which viral IAP precludes apoptosis in insect hosts. Viral IAP interacts with and stabilizes the host’s IAP, keeping the host IAP active preventing caspase activation and apoptosis. The Friesen Lab’s paper on this finding is the first report of a viral IAP functioning in conjunction with the host IAP for the virus’s benefit. They hypothesize that viral IAP reduces auto-ubiquitination by decreasing the effect of an N-terminal degron in the host IAP.