In line with the aforementioned loss-of-function studies, Zhang et al. showed that overexpression of ADAR1 could inhibit ZBP1 activation through Z-RNA editing, thereby preventing ZBP1-mediated programmed necrosis of cells and tumor immune activation.4 Conversely, targeted inhibition of ADAR1 can improve the activity of ZBP1 and activate RIPK3-MLKL-dependent programmed necrosis to enhance the efficacy of tumor immunotherapy. Here, RIPK3 is linked to neoplasm.