Increased ER stress and the unfolded protein response (UPR) have emerged as driving forces for VSMC phenotypic transition and cell death in vascular disease.33,34 While the expression of ER/UPR markers increased during Ang II-induced AAA development (Supplementary Fig. 1d, e), Western blot analysis revealed a sharp downregulation of the expression of HSPA5, P4HB, ATF4, and ATF6, as well as the apoptosis marker cleaved caspase-3 (cl-CASP3), in KOs (Fig. 1g, h). The gene discussed is ATF4; the disease is triple-A syndrome.