In addition, modeling CAVD in endothelial cells differentiated from hiPSCs by introduction of the NOTCH1 mutations from patients with BAV and aortic valve stenosis has found that the NOTCH1 haploinsufficiency leads to the alteration of epigenetic architecture, resulting in derepression of latent pro-osteogenic and proinflammatory gene networks (139). This evidence concerns the gene NOTCH1 and congenital bilateral aplasia of vas deferens from CFTR mutation.