In regard to liver it has been recently demonstrated that the NLR family members NLRP6/NALP6 and NLRP-3 in conjunction with IL-18 negatively regulate progression of non-alcoholic fatty liver disease [14] and that the application of endotoxins including lipopolysaccharide (LPS) or fatty acids results in increased IL-1β production and strong activation of the NLRP-3 inflammasome [15,16]. Here, NLRP3 is linked to metabolic dysfunction-associated steatotic liver disease.