Many of the “dogmas of the quiet past”1– have given way to more well-founded concepts of disease in recent decades, as clinical science developed more precise investigative tools and effective therapies. Some dogmas have remained intact. One of these holds that high-altitude pulmonary edema (HAPE) is unknown2– or rare3 below 8,000 to 9,000 feet (2,440 to 2,745 m). Cases of HAPE at lesser altitudes are attributed to preexisting diseases such as skeletal or pulmonary vascular abnormalities.3–4 In the current issue of CHEST (see page 49), however, Gabry et al describe 52 lowlanders who acquired HAPE after skiing at 1,400 to 2,400 m between 1992 and 2000. This remarkable account of previously healthy persons is all the more noteworthy because the skiers slept at a mean altitude of 1,300 m. (As Hultgren,3 points out, HAPE is usually attributed to altitude of repose, rather than that of daily activity.) Whereas the altitude exposure of these skiers was much more mild than that of previous reports, their illnesses were not. The symptoms, cardiorespiratory signs, and radiographic abnormalities—83% of the patients had bilateral shadows extending over at least half of each lung—were severe. Gas exchange was equally deranged: the mean alveolar-arterial oxygen difference was 45 mm Hg. It is thus no surprise that these persons sought emergency medical care at the nearest hospital in Moutiers. This is a town of approximately 5,000, nestled 500 m (approximately 1,640 feet) above sea level, in the valley where the Isere River wends its alpine way through the Tarentaise region of southeastern France. Some of the tallest peaks in Europe are nearby. For example, Mont Blanc (15,760 feet/4,807 m) is within 45 km (< 30 miles). But these lofty heights are not readily accessible from Moutiers since the mountain passes are impassible in winter. Although the patients documented by Gabry et al skied only at lower altitudes, they became very ill nonetheless.