Our data suggests that EC dysfunction is present in these patients, and future research should focus on the role of endothelial dysfunction in the pathogenesis of BAV and the related aortic valve calcification and aortic dilation, taking into account the role of BAV related genes that are known to affect cell migration, proliferation, EndoMT and calcification such as SMAD6, NOTCH1 or TGFβR1 [1,2] [38,39,40,41]. This evidence concerns the gene TGFBR1 and aortic valve calcification.