Notably, myeloid‐specific SENP3 deficiency was associated with a significantly decreased incidence of AAA formation after AngII infusion (40% [12 of 30] of ApoE−/−;Senp3△Mø mice compared with 70% [21 of 30] of ApoE−/−;Senp3flox/flox mice; p < 0.05) (Figure 2H). This evidence concerns the gene AGT and triple-A syndrome.