Endometrial cancer (EC) is the most common cancer of the female genital tract, resulting annually in 76,000 related deaths worldwide. EC originates either from oestrogen-related proliferative endometrium (type I, endometrioid), or from atrophic endometrium (type II, non-endometrioid). Each type of EC is characterized by different molecular profile alterations. The Kirsten rat sarcoma viral oncogene homolog (KRAS) gene encodes a signalling protein which moderates response to various extracellular signals via down-regulation of the mitogenactivated protein kinase (MAPK) or phosphoinositide-3-kinase/vakt murine thymoma viral oncogene (PI3K/AKT) pathways. This article reviews the role of KRAS in predicting transition from hyperplastic endometrium to early-stage well-differentiated EC, as well as further invasive proliferation of the tumour to advanced-stage disease. KRAS seems to be directly associated with type I EC, and most studies support its early involvement in carcinogenesis. Current evidence correlates KRAS mutations with increased cell proliferation and apoptosis, as well as upregulation of endometrial cell oestrogen receptors. Tumours positive for KRAS mutation can harbour hypermethylation-related changes in genome expression, and this can be the cause of concurrent loss of DNA repair proteins. Despite some evidence that KRAS mutation status affects cancer progression, a consensus is yet to be reached. Based on the available evidence, we suggest that screening for KRAS mutations in patients with hyperplastic endometrium or early-stage type I EC, may provide important information for prognosis stratification, and further provision of personalised treatment options. Endometrial cancer (EC) is the most common cancer of the female genital tract in developed countries (1). Each year 319,500 women are diagnosed with EC resulting in 76,000 deaths worldwide (2). EC develops from the inner lining of the uterine corpus (3), and it is currently divided into two types as firstly described by Llobet et al. (4). Type I tumours tend to be low or intermediate tumour grade; they overlap considerably (80%) with oestrogen-related endometrioid carcinomas. Contrary to type I, type II EC results from a sequence of genetic alterations occurring in atrophic endometrium; this can occasionally reflect a progression from polyps or pre-cancerous lesions to EC. Type II EC is mostly considered as non-endometrioid serous carcinomas (4); it tends to be high grade, deeply invasive into the myometrium, and of more advanced stage at presentation (4, 5). The estimated 5-year overall survival for patients with any type of EC is 81.5% (any stage) (6). Current Staging EC staging consensus keeps with the 2009 International Federation of Gynaecology and Obstetrics (FIGO) revised classification. Revised FIGO staging defines four stages 533 This article is freely accessible online.