More recently, the S-nitrosylation of cIAP1 (a positive regulator of the NF-κB signaling pathway), induced by the NO donor GTN (particularly at cysteine 571), appeared as a critical cornerstone for switching the cancer cell fate from TNFα/TNFR1-mediated cell survival (through the activation of the classical NF-κB cascade) to TNFα/TNFR1-mediated cell death [90]. The gene discussed is TNFRSF1A; the disease is cancer.