KRAS and neoplasm: The most frequent alterations in type I EC are: mutations in the phosphatidylinositol-4,5-bisphosphate 3-kinase (PIK3CA) pathway, with 90% of tumours showing loss of phosphatase and tensin homologue (PTEN) [144]; mutations in KRAS found in 20% of tumours [145]; mutations in fibroblast growth factor receptor 2 (FGFR2) in 12% of tumours [146]; amplification of human epidermal growth factor receptor 2 (HER-2) in some subtypes [147]; loss of DNA mismatch repair (MMR) proteins (found in hereditary Lynch syndrome) [148].