Our observations showing that inhibition of HDAC6 increases acetylation of Ku70 at lysine residue 539, known to abolish the ability of Ku70 to suppress Bax-mediated apoptosis34 and that Tubastatin A treatment enhances PAH-PASMC apoptosis, which is blocked by a Bax-inhibiting peptides derived from the Bax-binding domain of Ku70, strongly support the implication of Ku70 in vascular remodeling. Here, HDAC6 is linked to pulmonary arterial hypertension.