They noticed that follicular fluid exposure led to DNA double stranded breaks and, consequently, the stabilization of the tumor suppressor TP53. Early precursors of high grade serous ovarian cancer are also defined by their high expression of TP53 and high levels of DNA damage, although in the vast majority of these cases TP53 is also mutated, often with a gain of function mutation[71]. This evidence concerns the gene TP53 and ovarian serous adenocarcinoma.