RIP1 kinase activity is crucial for necroptosis induced by Fas, TNF and TRAIL death receptors,34 and Nec-1, an allosteric inhibitor of RIP1 kinase, abolishes necroptosis-specific RIP3 phosphorylation and inhibits death receptor-induced necroptosis in different cellular models.35 In our study, Nec-1 partially rescued ovarian cancer cells from ARHI-mediated cell death by 40–50% (Figure 4d). This evidence concerns the gene FAS and ovarian carcinoma.