Since in this study, active RIP3 did not proceed to necroptosis execution in the lungs, and since both RIP3 and MLKL has previously been indicated to mediate activation of NLRP3 inflammasome independently of necroptotic cell death,13, 14, 15 we sought to identify additional RIP3‐dependent pathways which might underlie this tissue injury due to PAH. Here, NLRP3 is linked to pulmonary arterial hypertension.