For example, experimental stroke models have revealed that heightened barrier permeability observed at 4–12 h post-stroke is attributable to elevations in caveolin-1 expression, driving changes in the transcellular pathway, followed by later disruption at 24–48 h due to dysregulation of TJ proteins occludin, claudin-5, and ZO-1, which initiates changes in the paracellular pathway [54,55]. The gene discussed is OCLN; the disease is stroke disorder.