Similar evidence shows that although NLRP3 expression is increased in RAW 264 cells infected with A. actinomycetemcomitans, it may not be the most vital player in promoting inflammatory bone loss in this scenario: inhibition of ROS and cathepsin B rather than Nlrp3 knockdown can prevent increased IL-1β secretion, and the bone resorption activity of osteoclasts differentiated from Nlrp3-deficient macrophages of mice with experimental periodontitis induced by A. actinomycetemcomitans is even increased (250, 251). The gene discussed is NLRP3; the disease is periodontitis.