In vitro studies suggest hypoxia-reperfusion injury affects the subcellular localisation of the proteins zona occludens 1, occludin and claudin-5 and their association with tight junction complexes.3–5 However, when studied in vivo in an embolic model of stroke, tight junctions appear intact even in vessels showing BBB breakdown.6 Similar findings have been made recently in a transgenic mouse strain whose endothelial tight junctions are labelled with eGFP, allowing the dynamics of tight junction integrity to be monitored longitudinally in vivo. The gene discussed is OCLN; the disease is Stroke.