Although p16INK4A is a major senescence marker and our results reveal that (1) the levels of p16INK4A are higher in IPAH patient PAECs (Figure 1), (2) knockdown of p16INK4A in ECs prevents hypoxia-induced accumulation of αSMA-positive cells and increases in RVSP (Figure 2), and (3) knockdown of p16INK4A in ECs also decreases TWIST1 and PDGFB expression under hypoxia (Figures 2, 3), p16INK4A was not significantly differentially expressed in ECs isolated from hypoxia-treated mouse lungs in our bulk RNAseq analysis. This evidence concerns the gene CDKN2A and idiopathic pulmonary arterial hypertension.