These results suggest that the reduction in hyper-inflammatory cytokines by TRPV4 blockade attenuates endothelial dysfunction, thereby protecting against sepsis-associated pathophysiological processes that lead to a proinflammatory and procoagulant state of the endothelium, impaired regulation of vascular tone and increased permeability, leading to hypotension, hypoperfusion and edema formation, which ultimately cause organ dysfunction and death. The gene discussed is TRPV4; the disease is endothelial dysfunction.