Along with inflammation and immune response, lipid metabolism and its related functions (e.g., free radical scavenging, endocrine system development and function) were highly impaired at 1 and 2 dpi after experimental infection, dysregulating retinoid X receptor (RXR) related pathways such as LPS/IL-1 mediated inhibition of RXR function, LXR/RXR activation, FXR/RXR activation and hepatic cholestasis. The gene discussed is IL1A; the disease is infection.