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. 2023 Aug 23;55(8):1632–1643. doi: 10.1038/s12276-023-01069-y

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© The Author(s) 2023

Open Access This article is licensed under a Creative Commons Attribution 4.0 International License, which permits use, sharing, adaptation, distribution and reproduction in any medium or format, as long as you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons license, and indicate if changes were made. The images or other third party material in this article are included in the article’s Creative Commons license, unless indicated otherwise in a credit line to the material. If material is not included in the article’s Creative Commons license and your intended use is not permitted by statutory regulation or exceeds the permitted use, you will need to obtain permission directly from the copyright holder. To view a copy of this license, visit http://creativecommons.org/licenses/by/4.0/.

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Fig. 3 — TNF ligation or LPS stimulation results in activation of NF-κB signaling. Inactivation of NF-κB signaling or engagement of death receptors triggers the assembly of an apoptosis-inducing complex consisting of FADD, caspase-8, and RIPK1. When caspase-8 is inhibited, RIPK1 and RIPK3 form necrosomes through homotypic interactions with RHIM, resulting in phosphorylation of MLKL. Phosphorylated MLKL undergoes oligomerization and induces membrane rupture.