Experimental animal studies demonstrated that activation of the NF-κB transcription factor and the NLRP3 inflammasome are involved in a chronic inflammatory response to high oxidative stress in T2DM, which leads to an increase in IL-1β and IL-18, playing a crucial role in the development of diabetes [58], aggravating pro-coagulant activity [6]. This evidence concerns the gene IL18 and diabetes mellitus.