Utilizing in situ imaging and HE staining, we observed that the activation of the STING pathway led to an enlargement of the plaque area in both GSDME−/−/ApoE−/− and ApoE−/− mice, thereby counteracting the suppressive influence of GSDME deficiency on atherosclerosis progression (Figure 4A,C). This evidence concerns the gene APOE and atherosclerosis.