In this study, we also showed that the ERK–MAPK pathway was activated in 15 (33.3%) out of 45 ovarian carcinomas and activation depended on the mutational status of KRAS and BRAF. This is in contrast with a recent report showing that this pathway is frequently activated independent of the status of KRAS and BRAF in endometrioid-type endometrial cancer (Mizumoto et al, 2007). This evidence concerns the gene BRAF and endometrial cancer.