Moreover, our previous study demonstrated that hyperglycemia, a hallmark of T2DM, could induce reactive oxygen species (ROS)-sensitive NLRP3 inflammasome activation in human monocytes (10), suggesting that high glucose (HG) is a key factor of activated innate immunity in T2DM, which could be sensed by NLRP3 inflammasome and mediate the processing of IL-1β under diabetic condition. This evidence concerns the gene IL1B and type 2 diabetes mellitus.