In a Con A-induced mouse model of hepatitis, it was discovered that a decrease in the relative amount of Clostridium in the intestinal tract and a concomitant reduction in the number of secondary bile acids secreted by Clostridium attenuated liver injury by inhibiting its activation of the G protein-coupled bile acid receptor 1 (GPBAR1) on the surface of natural killer T (NKT) cells and suppressing their polarization to NKT 10 cells and the secretion of IL-10 (Biagioli et al., 2019). This evidence concerns the gene GPBAR1 and hepatitis A virus infection.