Consequently, during aging, dysregulation and lower levels of BMAL1 may explain the increase in the prevalence of disc calcification by activating TGF/BMP signaling, as noted in ligamentous tissues.138 Supporting this crucial role of Bmal1 contribution to disc calcification, ank mutant mice with dysregulated BMAL1/CLOCK signaling showed similar dystrophic mineralization of the AF. This evidence concerns the gene CLOCK and atrial fibrillation.