To determine if inhibition of TRPV4 channels protects against cytokine-induced endothelial dysfunction, we measured the abundance of circulating factors indicative of a general level of endothelial activation—a pro-inflammatory and pro-coagulant endothelial cell state that promotes endothelial dysfunction—in mice treated with LPS or LPS+GSK219. The gene discussed is TRPV4; the disease is endothelial dysfunction.