While tightly regulated cellular activation and NO production in the brain and other organs promote self-healing following sublethal infection with OtK [15,16], we believed that OtK-mediated cell death and uncontrolled type-1 inflammation collectively lead to rapid and progressive loss of Tie2 and tight junctions and endothelial barrier function, leading to host death (Figs 1 and 5). The gene discussed is TEK; the disease is infection.