Amid several molecular events causative of drug resistance in ovarian cancer, more than 10% cases of ovarian cancer patients (n = 489) exhibit copy number amplification of oncogenes such as cyclin E1 (CCNE1), Kirsten-rat sarcoma virus (KRAS), MDS1–EVI1 complex locus (MECOM), and Mitogen-activated protein kinase 1 (MAPK1) exemplifying their potential as therapeutic targets [3–5]. This evidence concerns the gene KRAS and ovarian cancer.