Because RPLS is attributed to hypertensive encephalopathy and endothelial dysfunction leading to breakdown of the blood-brain barrier, focal cerebral oedema, or vasospasm, inhibition of VEGF signalling is implicated in the pathophysiology, but the syndrome often has other contributing factors and has not yet been replicated after VEGF inhibition in preclinical models. This evidence concerns the gene VEGFA and endothelial dysfunction.