AVP release stimulates V1a and V2 receptors, which then cause platelet aggregation, vasoconstriction, and water retention with low plasma osmolality and hypovolemic or euvolemic hyponatraemia as consequences with resultant infarct volume expansion. This is the first study we are aware of that looked into the relationship between copeptin level, ischaemic stroke severity, and infarct volume in the country [22,33,34]. This evidence concerns the gene AVP and ischemic stroke.