Further analysis indicated that TAGLN2 might promote PAH progression through immune and metabolic pathways: on the one hand, by activating HLA DR+ monocytes (mediation proportion 6.15%), it exacerbated pulmonary vascular inflammatory responses; on the other hand, by increasing the levels of eicosadienoic acid (mediation proportion 5.21%) and cysteinyl dipeptide (mediation proportion 3.15%), it induced oxidative stress and lipid metabolism disorders. The gene discussed is TAGLN2; the disease is pulmonary arterial hypertension.