HA modulation of TNFα-induced function, particularly the oxidative burst, is intriguing considering that enhanced ROS production at the inflammatory site is commonly thought to contribute to the progression of numerous inflammatory diseases (73), including rheumatic diseases driven by TNFα with concomitant ECM degradation, such as rheumatoid arthritis and vasculitis (82, 83). The gene discussed is TNF; the disease is vasculitis.