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). This evidence concerns the gene IL6 and diabetes mellitus.