In Type I endometrioid adenocarcinoma, mutations in PTEN, K-Ras, and β-Catenin lead to the activation of key pathways such as PI3K-Akt, MAPK, and Wnt, which promote CCND1 overexpression through β-Catenin-mediated TCF/LEF transcription and activation of c-Myc [13,14,15,16]. Here, KRAS is linked to endometrioid adenocarcinoma.