COL1A1 and congenital bilateral aplasia of vas deferens from CFTR mutation: With cellular trajectory analysis from single-cell RNA-seq of aortic valve leaflets in calcific aortic valve disease (CAVD) patients, it has been reported that valve endothelial cells may participate in the calcification and thickening of aortic valve disease though more active EndoMT, demonstrated by greater expressions of secreted protein acidic and rich in cysteine and mesenchymal markers (Col1A1 and Cnn1) in transformed valve endothelial cells of CAVD patients than healthy controls (Kang et al., 2020).