TP53 loss and BRCA1/2 alterations are characteristic and presumed initiating events in carcinogenesis in high-grade serous ovarian cancer, whilst PI3K/AKT/PTEN pathway hyperactivation is presumed to play a role in part of endometrial ovarian tumors and in the development of germ cell tumors [20–22]. This evidence concerns the gene TP53 and testicular germ cell tumor.