We reported that in many subtypes of AML, especially in M4 and M5, the anti-leukemia effects of NF-κB inhibition are attenuated by autocrine TNF stimulation of JNK (a survival/proliferation signal in LCs) and paracrine TNF stimulates a JNK-mediated necroptotic/apoptotic signal in HSPCs [16]. Here, TNF is linked to acute myeloid leukemia.