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. Here, TP53 is linked to neoplasm.