Although we could detect neither TLR9 nor inflammasome activation in Ku80-deficeint VSMCs (data not shown), we observed marked increases of cytosolic DNA fragments (Fig. 5A,B), cGAMP concentration (Fig. 5C), TBK1 phosphorylation (Fig. 5D), and proinflammatory cytokine expression in Ku80-deficient VSMCs (Fig. 4A), which indicate that the accumulation of DSBs and resultant cytosolic DNA fragments induced cGAS-STING activation and subsequent inflammatory responses, thus contributing to atherosclerosis development. This evidence concerns the gene CGAS and atherosclerosis.