Aneurysmal subarachnoid haemorrhage (aSAH) is a severe subtype of stroke, mediated by the spontaneous rupture of an intracranial aneurysm, that frequently occurs in people between 40 and 60 years of age. Cerebral vasospasm (CV), and related delayed cerebral ischemia (DCI), is a clinical syndrome of the focal neurologic deficits that develop typically three to fourteen days after the aneurysm rupture, and is a major cause of death and disability after aSAH. Vascular constriction and inflammation, more specifically leukocyte-endothelium interaction, appear to play a critical role in CV. Although the main focus of pharmacological treatment of aSAH is the prevention of DCI, the only pharmacological drug shown to reduce the risk of DCI and unfavourable outcome is nimodipine, an L-type Ca2+ channels (LTCCs) antagonist, which does not alter the incidence or severity of CV [1]. On the other hand, although inflammatory biomarkers that facilitate leukocyte-endothelium interaction have been found in the cerebral spinal fluid and serum of patients [2], none of these biomarkers have been shown to be useful tools for predicting CV development or outcome after aSAH. Therefore, it is necessary to study new pathophysiological pathways to improve outcomes and management of patients.