In contrast to its role in occlusive vascular disease by inhibiting VSMC migration into the intimal space through sequestering the scaffold protein p130Cas at focal adhesions [19], CRP2 mediated Ang II-activated Erk1/2 signaling pathways, thereby causing aberrant aortic ECM remodeling and AAA formation. The gene discussed is CRIP2; the disease is triple-A syndrome.