Figure 3 connects LPS and IFN–γ to NEK2 levels. LTA exerts immune-stimulating activities to induce NO production in mouse macrophages primed with IFN-γ, suggesting that it exerts a pivotal role in the pathogenesis of inflammation [29]. When the endothelial monolayer becomes leaky and inflamed, it allows for an excessive flux of innate immune cells and humoral effector molecules to cross the micro-vessel wall to the surrounding tissues. Endothelial barrier dysfunction has been associated with inflammatory lung disease and sepsis [22]. This evidence concerns the gene IFNG and Sepsis.