It has been demonstrated that a low level of ROS positive regulate the priming signal of the NLRP3 inflammasome and promote NLRP3 inflammasome activation; however, Erttmann and Gekara demonstrated that a high level of ROS release by Streptococcus pneumonia increased the oxidative levels of the inflammasome components ASC and caspases and inhibited the NLRP3 inflammasome (24). This evidence concerns the gene NLRP3 and streptococcal pneumonia.