As an example, immunopathologic vasculopathy in a hypoxic model of pulmonary hypertension was found to be driven by G6PD-induced pro-inflammatory epigenetic signaling — including upregulated expression of pro-inflammatory factors (e.g., tumor necrosis factor-alpha [TNF-α]), increased numbers of activated macrophages, and activated platelets — and conversely, was able to be mitigated with G6PD deficiency (15, 16). This evidence concerns the gene G6PD and pulmonary arterial hypertension.