Growing evidence has demonstrated that the PI3K–Akt pathway is a central mechanism controlling CSC features in various cancers including endometrial cancers and is strongly related to a malignant phenotype.35, 36, 37, 38 We previously demonstrated that inhibition of the MAPK pathway rescued endometrial cells from apoptosis, whereas PI3K inhibition promoted apoptosis in immortalized rat endometrial cells expressing activated KRAS proteins.39 Our present findings suggest that DUSP6 expression leads to inactivation of MAPK–ERK1/2 signaling and activation of PI3K–Akt. This evidence concerns the gene AKT1 and cancer.