BCL2L11 and neoplasm: At the level of tumor immune surveillance, IFN-I induce programmed tumor cell apoptosis by upregulating TRAIL and its receptors and activating caspase-8 (166, 167); promoting mitochondrial depolarization, decreasing Bcl-xL while increasing Bim and PARP-associated signals with AIF translocation (168), and enhancing DC maturation, antigen cross-presentation, and CD8+ T-cell expansion (169).