For instance, upon cytosolic exposure to Shigella bacteria, XIAP is activated to promote an inflammatory response to clear the infection; However, Shigella has evolved a strategy to escape the innate immune defense by Bid-activation, which in turn potentiates the release of mitochondrial second mitochondria-derived activator of caspases to neutralize XIAP-mediated inflammatory signaling [18]. Here, XIAP is linked to infection.