STUB1 and congenital bilateral aplasia of vas deferens from CFTR mutation: Pathways analysis revealed that CAVD patients without CHIP in comparison with non-calcific controls show disruption in multiple pathways including, Th1, Th2, and NK cell signaling, leukocytes extravasation, phagosome activation, atherosclerosis signaling, and inhibition of matrix metalloproteases (Fig. 3a, right panel).