A comparable protection was conferred by necrosulfonamide, a pharmacological inhibitor of MLKL [27] in the same subset of tumor cell lines that we had used for analysis in Figure 3a (Figure 3g), being furthermore in line with a recent study from Wu and coworkers who found that TRAIL/zVAD/CHX-induced programmed necrosis is compromised considerably in MLKL-deficient mice [27], and in summary identifying MLKL as a mediator not only of TNF/zVAD/CHX-, but also of TRAIL/zVAD/CHX-induced programmed necrosis. This evidence concerns the gene MLKL and neoplasm.