Regarding the relevant mechanism by which GPBAR1 mediates anti-inflammatory in cholestasis, in the macrophages of GPBAR1-KO mice, the RNA levels of various proinflammatory genes, such as inducible nitric oxide synthase (iNOS), interferon-inducible protein and IL-1, which are targeted by NF-κB, were higher than those of WT mouse macrophages, suggesting that the anti-inflammatory effect of GPBAR1 is mediated by inhibiting NF-κB (Calmus and Poupon, 2014) (Figure 3). Here, NFKB1 is linked to cholestasis.