In TNF-α-treated rPAECs, overexpression of miR-181a/b inhibited the increase in endoglycans in TNF-α-treated cells and also inhibited the action of TNF-α, together confirming that miR-181a/b plays a negative regulatory role in PAH by mitigating the inflammatory response through interaction with endogenous glycans [42]. This evidence concerns the gene TNF and pulmonary arterial hypertension.