Two recent studies have reported a role for NINJ1 in models of liver damage in mice, caused by LPS plus D-galactosamine, concanavalin A, Jo2 anti-Fas agonist antibody, or ischemia-reperfusion injury.132,133 One of these studies also demonstrated that anti-NINJ1 neutralizing antibodies, which prevent NINJ1 oligomerization, significantly reduced circulating DAMPs, including IL-18, HMGB1, mitochondrial DNA, and markers of liver inflammation.133 However, further characterization of NINJ1 in vivo is needed to fully assess its physiological significance. This evidence concerns the gene NINJ1 and inflammatory response.