With regard to the mechanism of double positivity, p16 is frequently overexpressed in high-grade serous ovarian cancer, and <1% of these tumors harbor a CDKN2A mutation, so p16 overexpression is thought to be secondary to dysregulation and to underlying p53 and/or Rb mutations [54]. This evidence concerns the gene CDKN2A and ovarian serous adenocarcinoma.