Subsequently, IL-1β is synthesized as an inert pro-protein and is cleaved by caspase-1, a cysteine protease domain of the NLRP3 inflammasome, to yield the mature, bioactive form of IL-1β in response to various obesity-induced intracellular stressors, such as ROS accumulation (reviewed in [291,292]) (shown in Figure 2; discussed in Section 6.3). The gene discussed is IL1B; the disease is obesity due to melanocortin 4 receptor deficiency.