As stated above, like many other protein fragments, fragmented RIPK1, bearing Cys at its N-terminal, has been shown as N-end rule substrate and it degrades via Arg-ATE1 N-end rule pathway.14 This RIPK1 (receptor interacting serine-threonine protein kinase-1) is one of the key regulators of necroptotic cell death.33 Necroptosis or programmed necrosis is recently emerging as an alternate therapeutic modality for apoptosis-resistant cancer cells and its initiation requires the activation of RIP1 and RIP3 kinases. The gene discussed is RIPK3; the disease is cancer.