Apoptosis escape due to the upregulation of proteins implicated in the intrinsic (mitochondrial) pathway, including members of the B cell lymphoma 2 (BCL2) superfamily (e.g., BCL2, MCL1, BCL-xL/BCL2L1, BFL1/BCL2A1 anti-apoptotic proteins) and of the inhibitor of apoptosis (IAP) family (e.g., NAIP/BIRC1, cIAP1/BIRC2, cIAP2/BIRC3, XIAP/BIRC4, and survivin/BIRC5), may contribute to the development of drug resistance in many cancer types, including AML [14,15,16,17]. Here, XIAP is linked to acute myeloid leukemia.