While we show that ERK1/2 mediates thrombin-induced endothelial barrier disruption (Fig. 5B), consistent with its role in endothelial inflammation (40, 41), it remains to be determined how crosstalk between p38 and ERK1/2 signaling impacts endothelial dysfunction in response to GPCR stimulation. Here, MAPK14 is linked to endothelial dysfunction.