Exogenous expression dnMCAK (a promoter of CCF) [38] in the breast cancer cells treated with H3K9me2 and H3K27me3 inhibitors increased the formation of CCF and suppressed the reduction of SASP and inhibition of cGAS-STING signaling mediated by dual inhibition of H3K9me2 and H3K27me3, as indicated by increased p-STING, IL-6, and IL-8 levels (Figure 4D). This evidence concerns the gene CGAS and breast carcinoma.