In general, many additional pro-inflammatory mediators controlled by NF-κB p65 are known (e.g., TNF-α, IL-1β, IL-6 and MCP-1 [45]) and their contribution to the observed effects of Aqp9 deletion on the survival to endotoxemia can be anticipated. The gene discussed is AQP9; the disease is serum lipopolysaccharide activity.