Given these facts that TNFα is produced upon exposure to bacterial components such as lipopolysaccharide (LPS) and other endotoxins, TNFα is stimulated by microbial pathogens for orchestrating anti-microbial responses, and TNFα inhibitory biologic agents render users at a raised risk of serious infection [9]–[11], it is conceivable that TNFα blockers or antagonists should ameliorate RA by abolishing infection-evoked TNFα, and also logically reasonable that the onset of RA is likely attributed, in part, to microbial pathogens. The gene discussed is TNF; the disease is rheumatoid arthritis.