Firstly, HG enhanced autophagy in the short term (0-12 h) in a dose-dependent manner and negatively regulated ROS-NLRP3 inflammasome signaling, while continuous and chronic hyperglycemia actually inhibited the level of autophagy, resulting in increased expression of ROS, caspase1, and IL-1β. The gene discussed is NLRP3; the disease is Hyperglycemia.