Subsequent studies would evaluate effects on target pathogenic mechanisms which may be shared with other PAH etiologies (i.e., TGF-β signaling, with an agent like sotatercept) or mechanisms that are thought to be unique to SchPAH (i.e., potentially Th2 inflammation and TSP-1 expression on Ly6c+ monocytes). Here, THBS1 is linked to pulmonary arterial hypertension.