A pool of survivin is recruited to mitochondria, mostly of tumor cells and released in the cytosol in response to cell death stimuli. Mitochondrially released survivin forms a complex with XIAP that is negatively regulated by protein kinase A (PKA) phosphorylation of survivin on Ser20, and results in increased XIAP stability against proteasomal degradation, enhanced gene expression, i.e. NF-κB, and synergistic inhibition of effector and initiator caspases (a schematic diagram of caspase 9 is shown).