Subtle or initial reduction in oxygen diffusion may induce short-term response mechanisms by Cav-1/caveolae mechanosensor function, like eNOS modulation and lung capillary dilation; the persistence of hypobaric hypoxia may conduct Cav-1 delocalization from caveolae, co-adjuvated by HIF2α-mediated cholesterol reduction, and subsequently reductions of its expression, leading to pathological scenarios like pulmonary hypertension and hypobaric hypoxia-induced pulmonary edema (Figure 4). This evidence concerns the gene CAV1 and pulmonary edema.