Interestingly, although activating point mutations in KRAS in ovarian cancer are observed predominantly in low grade serous subtype and rarely in high grade cases, of the 25 samples with an amplification at KRAS of at least 0.8 (log2) in amplitude, all but one were high-grade serous, suggesting an alternative mechanism for activation of this pathway in a subset of high grade serous carcinomas. This evidence concerns the gene KRAS and ovarian carcinoma.