Indeed, LPS is a potent activator of NLRP3 inflammasome (signal 1), and it is tempting to hypothesize that the interaction between gut microbiota, NLRP3 inflammasome with the induction of enhanced release of inflammatory cytokines like IL-18, LPS and TMAO could be operating in various relevant obesity-related disorders including atherosclerosis and obesity induced myocardial remodeling. The gene discussed is NLRP3; the disease is obesity due to melanocortin 4 receptor deficiency.