Type 2 diabetes is associated with low-grade systemic inflammation [1]–[4], and increased levels of circulating proinflammatory mediators, e.g. tumour necrosis factor-alpha (TNFα) and gut-derived lipopolysaccharide (LPS), may play a role in the pathogenesis of insulin resistance, the hallmark of type 2 diabetes [5]–[8]. The gene discussed is TNF; the disease is type 2 diabetes mellitus.