Specifically, increased oxidative stress initially inactivates several enzymes by the formation of adducts with lipid peroxidation products such as HNE [115]; one such enzyme is OGG1, which during increased oxidative stress becomes a transcriptional coactivator for transactivators such as NFκB [35], enhancing expression of several inflammatory genes, including cytokines that enable transformation of the tumor microenvironment, and other proteins that protect cancer cells from the immune system, despite activation of several types of immune cells [56]. This evidence concerns the gene NFKB1 and neoplasm.