Interestingly, the acetylation level of α-Tubulin, a substrate of HDAC618, was not changed between control and PAH-PASMCs (Supplementary Figure S1) suggesting that the increased activity of HDAC6 in these cells is counterbalanced by histone acetyltransferases as previously observed in other diseases29. This evidence concerns the gene HDAC6 and pulmonary arterial hypertension.