SMAD3 and infection: In other barrier models, e.g., in blood–brain barrier models, it has been shown that the production of inflammatory factors contributes to the dysfunction of the endothelial and/or epithelial barriers after pathogen infection and the activation of many signaling pathways such as TNF signaling, TGF-beta signaling, SMAD3 signaling, STAT5 signaling, HIF-1 signaling pathway, EGFR tyrosine kinase inhibitor resistance, and MAPK signaling pathway, all of which are involved in regulating the production of inflammatory factors and/or VEGF-A (32–37).