The SASP is characterized by the secretion of pro-inflammatory cytokines (e.g., IL-6, IL-1β, TNF-α), matrix metalloproteinases (MMPs), and reactive oxygen species (ROS), which create a pro-inflammatory microenvironment and contribute to pathological remodeling of the extracellular matrix, disruption of the endothelial barrier function, and promote endothelial dysfunction [18, 19, 40–42]. The gene discussed is IL1B; the disease is endothelial dysfunction.