Further analysis of the data brings forward Spock1, Serpine1, Mmp12 and Mmp14, all of which have previously been shown to induce permeability,31 contribute to pulmonary oedema,32 negatively regulate cellular adhesion to extracellular matrix and impact on endothelial functions33, 34, 35, 36 suggesting that these factors may and probably play an important role in permeability, endothelial fenestration and oedema. The gene discussed is SERPINE1; the disease is pulmonary edema.