This protein modification affects many cellular effectors, including JNK and ASK1 kinases, which are normally involved in the activation of apoptotic pathways, but are inhibited upon S-nitrosation, promoting the survival of cancer cells; Bcl-2 protein, which has an anti-apoptotic function; its stabilization by NO inhibits its degradation and further promotes cell resistance to cell death; PTEN, a tumor suppressor protein that inhibits the PI3K/Akt pathway; S-nitrosation leads to its inactivation, eliminating the anti-tumor mechanism [51,52,53]. This evidence concerns the gene TCHP and neoplasm.