On the basis of the respective roles of oxidative stress, inflammation, and IL-β in the pathogenesis of PAH, as well as the interactions between reactive oxidative species, the inflammasome, and IL-1β, we propose that the antioxidative effect of ARC on PAH may contribute to the inhibition of the NLRP3 inflammasome via oxidative stress inhibition. Here, IL1B is linked to pulmonary arterial hypertension.