The prevailing theory of the pathogenesis of bone loss in inflammatory bowel disease patients suggests that the increase in T-cell activity in the state of intestinal inflammation leads to an increase in the systemic release of numerous proinflammatory cytokines, such as interleukin-1, tumor necrosis factor, transforming growth factor-α, interleukin-6 and interleukin-4 [38–40]. The gene discussed is TNF; the disease is inflammatory response.