Evidence for this includes the frequent co‐existence of serous borderline tumours with low‐grade serous carcinomas,18 and similar molecular changes: both serous borderline tumours and low‐grade serous carcinomas commonly feature mutations in BRAF or KRAS,39 but rarely in TP53,40 in contrast to high‐grade serous carcinoma. This evidence concerns the gene KRAS and serous adenocarcinoma.