While significant steps were being made toward understanding the molecular mechanisms underlying S. aureus infection of the endothelium, considerable evidence to support the concept that immune and inflammatory mediators released at sites of infection, such as Tumour Necrosis Factor alpha (TNFα), Interleukin 1 beta (IL-1β) and interferon gamma (IFNγ), can act directly on endothelial cells to modulate function in pathologic processes. The gene discussed is IL1B; the disease is infection.