Activated nuclear factor kappa light-chain enhancer of activated B cells (NF-kB) signaling was found throughout the CAVD process in both VEC and VIC, and the genetic deletion of NF-kB activation attenuates CAVD through the inhibition of p65-mediated inflammatory endothelial-to-mesenchymal transition (EndMT) in VEC and VIC calcification [15]. Here, NFKB1 is linked to congenital bilateral aplasia of vas deferens from CFTR mutation.