TNFRSF1A and acute myeloid leukemia: Indeed, in accordance with the idea that this mirrors the ability of TNFR2 to sensitize for TNFR1-induced cell death signaling by restricting the availability of TRAF2-cIAP/1/2 complexes (see introduction), SMAC mimetics which deplete cIAPs by triggering their proteasomal autodegradation also sensitizes AML cells for autocrine TNF-mediated necroptosis [112].