By combining lineage-tracing models, scRNA-seq and scATAC-seq, Chakraborty et al. demonstrated that contractile VSMCs in murine AAD transition into an inflammatory VSMC state characterized by up-regulation of interferon-stimulated genes and chemokines; chromatin-accessibility analyses implicated a dsDNA–STING–TBK1–IRF3 signaling axis and specific enhancer reprogramming in driving this phenotypic switch, and pharmacologic inhibition of STING or TBK1 mitigated aneurysm formation and rupture [22]. Here, STING1 is linked to aneurysm.