While TP53 mutation is a key early event, we have not identified an event that would lead to a high rate of somatic mutations to initially inactivate TP53. Additional studies evaluating candidate mechanisms, such as APOBEC3B (46) are needed to understand initial carcinogenic events that lead to inactivation of TP53. Our data, which show that mutations in TP53 may be driver events in ovarian carcinogenesis, provide additional impetus for efforts to restore the function of TP53 or exploit its deficit in patients with HGS ovarian cancer. This evidence concerns the gene APOBEC3B and ovarian carcinoma.