Furthermore, various mouse models of AML with distinct genetic abnormalities showed that autocrine TNF production and TNFR activation by AML cells, especially leukemia-initiating cells, make a crucial contribution to tumor progression through NFκB and JNK-mediated survival signaling [105,106,107], which might antagonize tonic TNF-driven necroptotic signaling [108]. This evidence concerns the gene TNFRSF1A and acute myeloid leukemia.