Gao et al., through single-cell transcriptome analysis, identified upregulation of gasdermin D (GSDMD), a pyroptosis effector, in aortic VSMCs during angiotensin II-induced AAA, and further demonstrated in animal models that GSDMD promotes ornithine decarboxylase 1 (ODC1) expression via ER stress–CHOP signaling, with elevated putrescine levels mitigating AAA development, suggesting that putrescine is a potential biomarker or therapeutic target [108]. This evidence concerns the gene GSDMD and triple-A syndrome.