A possible reasoning for this is that p53 and BRCA1, known regulators of MAD2, are commonly mutated in high serous ovarian cancer (Tp53 mutation is ubiquitous in ovarian high grade serous carcinoma) and mutations in these genes are uncommon in other ovarian cancer subtypes such as mucinous, clear cell, endometrioid and low grade serous [11, 52]. This evidence concerns the gene MAD2L1 and ovarian carcinoma.