More than 96% of HGSOC patients carry pathogenic TP53 mutations.[15] In addition to well‐established roles in controlling cell‐cycle arrest, apoptosis, and DNA damage repair, TP53 mutations have been reported to impair cGAS/STING activation, downregulate MHC class I expression, suppress antigen presentation in tumor cells, and increase circulating immunosuppressive neutrophils.[16, 17, 18] These pathways controlled by TP53 mutations exert suppressive effects on both the innate and adaptive immune systems, promoting an immunologically “cold” tumor microenvironment in OC. The gene discussed is STING1; the disease is neoplasm.