At the molecular level, COVID-19-associated endothelial dysfunction is characterized by reduced nitric oxide (NO) bioavailability, increased oxidative stress largely driven by NOX2-mediated reactive oxygen species (ROS) production, and an upregulation of adhesion molecules such as vascular cell adhesion molecule 1 (VCAM-1) and intercellular adhesion molecule 1 (ICAM-1), facilitating leukocyte adhesion and transmigration [25]. The gene discussed is ICAM1; the disease is COVID-19.