Targeting homeostasis and repair/inflammation in critically ill patients is an attractive option and has already led to the development of new drugs [45, 158, 163] . From current knowledge, one can speculate about the best options for therapy aimed at the Ang/Tie system. In critical illness, Ang-1 is considered to be the 'good guy' because it can create vascular stability and thus its activity should be supported. In contrast, Ang-2 appears to be a 'bad guy' that induces vascular leakage, so its activity should be inhibited [164] .