In that context, it is interesting to note that the KRAS alteration profile in our study differed between histological subtypes, with high-grade serous carcinomas harboring only gain in one patient, while endometrioid and clear cell carcinomas harbored only mutations, most of which were located in codons 12 and 13.We observed that in some patients, postulated sensitivity to KRAS or MEK inhibitors was not based on KRAS alterations, but on NF1, NF2 or MEK alterations. The gene discussed is NF2; the disease is serous adenocarcinoma.