Epidemiologists have consistently found that chronically elevated plasma levels of systemic markers and potential mediators of inflammation and the acute-phase response such as C-reactive protein, fibrinogen, interleukin 6, tumor necrosis factor-alpha (TNFα), and macrophage migration inhibitory factor (MIF) are associated with an increased risk of future IR [4], [49], suggesting that factors that either elicit or contribute to chronic inflammation may participate in the pathogenesis of IR and DM2. This evidence concerns the gene TNF and myotonic dystrophy type 2.