Specifically, tat-induced endothelial dysfunction is instigated by dysregulation of ROS production and upregulation of interleukin-1 beta (IL-1β), MCP-1, vascular cell adhesion protein-1 (VCAM-1) and E-selectin expression through activation of the NF-κB signaling pathway, as demonstrated on HUVECs [75,86,87,88]. This evidence concerns the gene IL1B and endothelial dysfunction.