In the context of gout, a decrease in BA levels leads to attenuated FXR activity, consequently diminishes the inhibitory effect on NLRP3 and NF-κB signaling pathways and promotes enhanced activity and expression of intestinal XOD, thereby triggering inflammatory responses and elevated UA levels, which exacerbate the progression of gout (Figure 4). Here, NFKB1 is linked to gout.