To explore the functional role of RIPK3 in obesity and associated metabolic disorders, 6-week-old male C57BL/6 mice genetically ablated for Ripk3 (knockout, KO)20, and age- and sex-matched wild-type (WT) control mice were fed for 16 weeks with either normal chow diet (NCD) or a choline-deficient HFD (CD-HFD), which is known to efficiently recapitulate the key features of human metabolic syndrome and non-alcoholic steatohepatitis (NASH)21, 22. This evidence concerns the gene RIPK3 and obesity disorder.