In previously reported animal models of SARS, alterations in coagulation and intra-alveolar deposition of fibrin proceed in parallel and occur in a particularly complex scenario in which pro-inflammatory factors participate (IL-1, TNF-alpha, IL-6), pro-fibrotic (TGF, CTGF, PDGF), together with the increase expression of the urokinetic pathway with activation of both pro-fibrinolytic and anti-fibrinolytic genes. This evidence concerns the gene IL6 and severe acute respiratory syndrome.