Opposing effects of inflammation on cancer have been described. Acute inflammation usually counteracts cancer development, while chronic inflammation promotes cancer development. Just as inactivation of the p53 pathway may be universal in the neoplasia, the activation of the NFκB pathway may, conversely, be frequent in carcinogenesis, and a requirement for inflammation and promotion. TNF, a key pro-inflammatory cytokine when binding to TNF receptor 1 (TNFR1), may cause survival or apoptosis, dependent on biochemical modifications that determine the type of complex formed; one complex causes NFκB activation and gives a cell survival signal (pro-oncogenic), while the other (modified) complex recruits caspases and causes apoptosis (anti-oncogenic). Fas-ligand (FasL)–Fas interaction can also result in opposing effects on carcinogenesis due to similar mechanisms. While IL-6 counteracts apoptosis and can promote cancer development, interferons can increase DNA repair and stabilize p53, thereby be anti-oncogenic.