Accordingly, TNFR1-induced necroptosis typically is only observable when caspase-8 activation is compromised, for example, naturally by genetic alterations in tumor cells (Teitz et al., 2001) or pathogen-encoded factors (Mocarski et al., 2011), such as CrmA or vICA, or artificially by use of drugs or genetic engineering. The gene discussed is TNFRSF1A; the disease is neoplasm.