Reaction to injury can be seen as an attempt to maintain homeostasis under exceptional conditions. ECs can be affected by several noxious mechanisms. The Ang/Tie system is considered crucial in fine-tuning their reaction to injury and in containing that reaction. Ang-2-deficient mice cannot mount an inflammatory response to peritonitis induced chemically or with Staphylococcus aureus [125] , but they can mount a response to pneumonia, suggesting the existence of inflammatory reactions for which Ang-2 is not mandatory. Ang-2 sensitizes ECs to activation by inflammatory cytokines. In Ang-2-deficient mice, leucocytes do roll on activated endothelium but they are not firmly attached, owing to the lack of Ang-2-dependent upregulation of adhesion molecules and the dominance of Ang-1-regulated suppression of adhesion molecules [120] [121] [122] [123] 125] .