Although the specific mechanisms leading to the development of sickness behaviors in cholestatic liver disease are not yet fully understood, alterations in pro-inflammatory cytokine production (including TNFα and IL-6), cellular adhesion molecule expression on cerebral endothelial cells, production of the chemokine monocyte chemoattractant protein-1 (MCP-1) by brain microglia, and cerebral recruitment of inflammatory monocytes have been broadly implicated (31–33). Here, TNF is linked to Cholestatic liver disease.