In Cav-1(−/−) mice, LPS elevates neutrophil sequestration (16×), lung microvascular permeability K(f,c) (5.7×), and edema formation (1.6×) in sepsis, resulting in endothelial NO synthase (eNOS)-derived NO production [80], which confirms that Cav-1 negatively modulate eNOS [81], similar to LynTK, SrcTK, G-proteins, and Ras signaling [39]. This evidence concerns the gene NOS3 and Sepsis.