Approximately 7–12% of endometrial cancer with somatic mutation in the proofreading exonuclease domain of the POLE gene.2 This POLE mutation is associated with the disruption of the exonuclease activity required for proofreading function and results in a high mutational burden or “ultramutator” phenotype.18 Thus, the particularly high mutation rates of p190A in endometrial cancer may be caused, at least in part, by POLE proofreading defects. This evidence concerns the gene POLE and endometrial cancer.