As observed in the Su/Hx model, inhibition of HDAC6 with TubA significantly improved RVSP, mPAP, CO, TPR, RV hypertrophy, vascular remodeling (as assessed by medial wall thickness and percentage of occluded vessels) and cell proliferation/apoptosis imbalance in the MCT rat model (Supplementary Figure S9) reinforcing the view that HDAC6 is an essential component of vascular remodeling in PAH. The gene discussed is DNMBP; the disease is pulmonary arterial hypertension.