Interestingly, CRISPR-Cas9-mediated knockout of cGAS or STING, or treatment with a small-molecule inhibitor of cGAS, strongly reduced the viability of cells with acute CIN, indicating that cGAS-STING signaling enables the tolerance of TNBC cells to acutely induced CIN. The gene discussed is STING1; the disease is cervical squamous intraepithelial neoplasia.