CircChordc1 was found to be significantly deregulated in aneurysmal tissue compared to healthy arteries, and it was capable of converting VSMCs to a contractile phenotype and improving their growth by triggering waveform protein degeneration and boosting the GSK3/-catenin pathway, which inhibited aneurysm formation and minimized the chances of fracture in angiotensin II and CaCl2-induced AAA mouse models [72]. This evidence concerns the gene AGT and triple-A syndrome.