KLK1 levels have been reported to be reduced in patients with cardiovascular and renal disease.6 Low KLK1 levels are also associated with increased risk for first-ever stroke, stroke recurrence, and stroke mortality.14 As a consequence of the endogenous KLK1 deficit, the production of vasodilating BK will be reduced, although partially compensated by a reported upregulation of kinin B2 receptor in the ischemic brain hemisphere.15–17 KLK1 augmentation therapy could enhance cerebral perfusion through increased BK production. The gene discussed is KNG1; the disease is stroke disorder.