CTHRC1 and congenital bilateral aplasia of vas deferens from CFTR mutation: Combining scRNA-seq and network analysis led to the isolation of a disease-driver VICs population with procalcific potential from human CAVD tissue, while temporal proteomic profiling identified monoamine oxidase-A (MAOA) and collagen triple helix repeat containing-1 (CTHRC1) as potential therapeutic targets57.