The term “essential hypertension” was coined by Frank (1) almost a century ago by stating “Because in this disease the increase in tone of the small arteries in the whole body (which leads to an increase in blood pressure) is the primary event…I will, in the following, name this disease, essential hypertension (essentielle Hypertonie).” The concept of hypertension being essential (i.e., serving to force blood through sclerotic arteries to the target organs) remained alive and well into the 1970s, and statements like “For aught we know, the hypertension might be a compensatory mechanism that should not be tampered with even were it certain that we could control it” (2) and “May not the elevation of blood pressure be a natural response to guarantee a more normal circulation to the heart, brain and kidneys” (3) continued to appear in published reports and spook physicians. This concept also instigated fear that, in susceptible patients, blood pressure (BP) could be lowered too much. Hence, the reluctance of many physicians to expose patients to antihypertensive therapy is not surprising, because abrupt lowering of BP in hypertensive emergencies, paradoxically, can increase target organ disease such as renal failure, encephalopathy, and coronary ischemia and even directly cause heart attacks, stroke, and death (4). Gradually, however, the pendulum began to swing toward the other extreme, and the dictum, “the lower the better,” became the leitmotiv for most physicians treating hypertension. The large, thorough meta-analysis of Lewington et al. (5) corroborated and amplified this concept by stating that “usual BP is strongly and directly related to vascular (and overall) mortality without any evidence of a threshold down to at least 115/75 mm Hg.” Statements like these threatened to put an end to the “essentiality” of essential hypertension.