LRRK2 and cholestasis: Our data first revealed that in TAA-induced mouse models of ALF and HE, the survival rate was twofold higher in the control group than in the Lrrk2−/−-mice and that LRRK2 deficiency significantly aggravated TAA-induced acute hepatic inflammation, which featured, to varying degrees, large focal hepatocytic necrosis, abnormal morphology in residual hepatocytes, edema, hepatocytic degeneration, cholestasis, collapse of reticular fiber scaffolds, infiltration of lobular inflammatory cells, and significant increase of acute inflammatory factors in tissues and peripheral circulation.