These findings are likely relevant for human disease, as reduced Prdm16/PRDM16 expression and increased levels of Adam12/ADAM12 were found in the aortic tissues of both mouse and human AAAs.85 Moreover, Adam12 was required for the pro-apoptotic effects of PRDM16 deficiency in SMCs, suggesting that the association between PRDM16 and ADAM12 may play a key role in AAA formation.85 Here, ADAM12 is linked to triple-A syndrome.