To explore further the potential disease-modifying role of HAMP, we used a well-established experimental mouse model of AAA, in which AngII is delivered subcutaneously via a slow-release pump over several days.19–21 Furthermore, to specifically assess the contribution of SMC-derived HAMP, we generated mice harboring a conditional tamoxifen-inducible deletion of the hamp gene specifically in SMCs (Hampfl/fl, SMMHC-CreERT2+). The gene discussed is AGT; the disease is triple-A syndrome.