In animal high-altitude models of PAH, when rodents were exposed to incremental increases in exposure time to high-altitude at 10, 20, and 30 days, measured TNF-α levels in pulmonary arteries of these high-altitude exposed rodents were also proportionately increased with increased exposure, whereas TNF-α levels in rodents reacclimated to low altitude were measurably reduced [17]. The gene discussed is TNF; the disease is pulmonary arterial hypertension.