These are the effects of the increased contractile proteins (i.e., ACTN1, TNNI3, and TNNT2) observed in our 3D PAH EHTs, a consequence of impaired BMP signaling because of a BMPR2 mutation [5], or a result of preserved epigenetic/environmental information that is maintained in the iPSCs [30], which should be investigated in more detail in future studies. This evidence concerns the gene ACTN1 and pulmonary arterial hypertension.