A different approach to this problem would be to hypothesize that the elevation of proinflammatory cytokines (IL-1, IL-6, TNF-a), observed in conditions such as infections, diabetes, renal failure, or rheumatoid arthritis is capable of down-regulating the enzyme expression by mechanisms of intracellular signalization, as shown in in vitro and in vivo studies, alongside scarce clinical evidence (6,7). The gene discussed is TNF; the disease is infection.