In diabetic ulcers, IFN-γ and TNF-α stimulate local endothelial cells in the wound and promote the secretion of T-cell and monocyte chemokines and adhesion molecules while disrupting endothelial barrier integrity.[42] Their findings suggest that IL-1β, IFN-γ, and TNF-α act cohesively and may provide an important proinflammatory link between osteomyelitis and DFU.[43]. The gene discussed is IFNG; the disease is osteomyelitis.