We previously reported that DENV infection of ECs upregulates the TF coagulation receptor in endothelial vascular cells, which triggers the generation of hemostatic proteases (thrombin) favoring the activation of protease-activated receptors or PARs, which, in turn, induces signaling inflammatory pathways (via phosphorylation of MAPKs p38 and ERK1/2, by transcription of the NF-κB factor), thereby supporting the upregulation of adhesion VCAM-1 or pro-inflammatory molecules in ECs, being part of the pathogenic mechanisms for the vascular endothelial injury present in severe Dengue cases [54]. The gene discussed is MAPK3; the disease is dengue disease.