Despite this discrepancy, alterations in the NOTCH1 signaling pathway offer a proven mechanism for CAVD, and downstream mechanisms for valve calcification are similar for Notch1‐driven CAVD in mice and idiopathic CAVD in humans (Hutcheson et al. 2014; Chen et al. 2015; Clark et al. 2017). This evidence concerns the gene NOTCH1 and congenital bilateral aplasia of vas deferens from CFTR mutation.