Necroptosis is a form of programmed necrosis. Necroptotic stimuli promote the interaction of the RIP1 and RIP3 kinases under conditions in which caspase-8 is not active. This RIP1/RIP3 complex, known as complex IIb, mediates necroptosis.

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  • News and Views |

    RIPK1 plays a key role in several inflammatory and cell death signalling pathways. Understanding its regulation is pivotal for identifying diseases that might therapeutically benefit from RIPK1 inhibition. Recent studies now show that TBK1 and IKKε constitute a cell death checkpoint that restrains RIPK1 activation.

    • Klaus Heger
    •  & Vishva M. Dixit
    Nature Cell Biology 20, 1330-1331
  • Research Highlights |

    Seehawer, Heinzmann et al. show that lineage commitment in liver cancer is independent of oncogenic driver expression and is instead dictated by the type of cell death occurring in the nearby liver microenvironment.

    • Anna Dart
  • News and Views |

    The cytokine tumour necrosis factor (TNF) and the toll-like receptors (TLRs) coordinate immune responses by activating inflammatory transcriptional programs, but these signals can also trigger cell death. Recent studies identify the MAP kinase substrate MK2 as a key player in determining whether cells live or die in response to TNF and TLR signalling.

    • Andrew Oberst
    Nature Cell Biology 19, 1150-1152
  • News and Views |

    Cancer treatments often focus on killing tumour cells through apoptosis, which is thought to typically require mitochondrial outer membrane permeabilization (MOMP) and subsequent caspase activation. A study now shows that MOMP can trigger TNF-dependent, but caspase-independent cell death, suggesting a different approach to improve cancer therapy.

    • Brent E. Fitzwalter
    •  & Andrew Thorburn
    Nature Cell Biology 19, 1014-1015