Interestingly, proinflammatory cytokines, that is, TNF-α and IFN-γ, during infection, exacerbate the effects of rickettsiae on endothelial permeability, further suggesting that the changes in the barrier properties of vascular endothelium are likely due to a combinatorial effect of intracellular rickettsiae and immune responses mediated by and/or directed against the infected host cell [26]. The gene discussed is TNF; the disease is infection.