Using the aortic elastase-perfusion model, we investigated the impact of necroptosis deficiency on AAA progression in necroptosis-deficient transgenic mice, including RIPK1 kinase-inactive (Ripk1<sup>D138N/D138N</sup>), MLKL knockout (Mlkl<sup>-/-</sup>), and MLKL phospho-deficient (Mlkl<sup>AA</sup>) animals. Here, RIPK1 is linked to triple-A syndrome.