This novel finding builds upon prior in vitro and preclinical evidence of changes in GLUT1 expression under ischemic conditions.22,23 Therefore, the larger GLUT1 intensity per microvasculature in those with hypertension, may be a consequence of a compensatory mechanism aiming to maintain glucose supply upon reduced microvascular flow and/or glucose transport.24 Our findings showed that hypertensive individuals exhibit larger intensity of perivascular MMP9 in periventricular NAWM and WMH compared to age-matched controls. The gene discussed is SLC2A1; the disease is hypertensive disorder.