Previously, we have shown that reintroduction of p19Arf to cancer cells that harbor wild type p53 leads to the activation of the p53 apoptotic program, but when an IFNβ antiviral context is induced simultaneously, an alternative mechanism of cell death is unleashed acting in a caspase 3 independent manner and through the up-regulation of RIP3K, a critical mediator of necroptosis14. Here, CASP3 is linked to cancer.