CCNE1 and ovarian neoplasm: This finding could be explained by the intrinsic reliance of cyclin E-overexpressing HGSOCs on high levels of HR proficiency; indeed, since amplified cyclin E is a well-known oncogenic driver of unchecked replication which leads to replicative stress and great genomic instability, cyclin E-overexpressing ovarian tumors are strictly dependent on robust HR DNA repair mechanisms for their survival [73].