For example, in colorectal cancer response to cetuximab strongly correlates with mutational status of KRAS but the assumption that this translates to other disease settings is false: EGFR mutations are not predictive of response to treatment in patients with ovarian cancer [115] while in advanced gastric cancer KRAS and BRAF mutations are significantly lower, and also do not correlate with response to cetuximab [116]. This evidence concerns the gene KRAS and ovarian carcinoma.