This study also showed that SIN3a deceased HDAC1 activity and decreased histone methylation by reducing the enrichment of H3K27me3 at the BMPR2 promoter region by antagonizing the expression of EZH2 and also demonstrated that SIN3a increased TET1-mediated DNA demethylation of the BMPR2 promoter region, thus identifying the SIN3a/EZH2-H3K27me3/TET1 pathway axis as a changing epigenetic mechanism that involves BMPR2 expression and vascular remodeling in PAH [21]. The gene discussed is HDAC1; the disease is pulmonary arterial hypertension.