MLKL and neoplasm: Mechanistically, 7I elicits necroptosis via the canonical RIPK1/RIPK3/MLKL pathway while simultaneously activating the p53/p21/CDK1/cyclin B pathway to enforce G2/M arrest, thereby achieving potent tumor suppression and positioning 7I as a therapeutic candidate for glioblastoma (GBM) treatment [211].