Molecular alterations that occur in mucinous ovarian carcinoma include KRAS/NRAS mutations (65.8%), TP53 mutation (65.2%), ERBB2 amplification (26.7%) and BRAF mutation (8.7%).1 These gene mutations and the resulting proteins can be used to distinguish between normal cells and cancer cells and can serve as specific molecular targets for targeted therapy. This evidence concerns the gene KRAS and ovarian mucinous adenocarcinoma.