Hao et al [40] found that FXR gene knockout mice were more susceptible to lipopolysaccharide (LPS)-induced NLRP3 inflammation-associated sepsis, while FXR overexpression mice were more resistant to it, indicating that BA activation of the nuclear receptor FXR had an inhibitory effect on NLRP3 inflammation-related sepsis. Here, NR1H4 is linked to Sepsis.