Of the seven endometrial tumors that had somatic mutations in TNK2 and/or DDR1 in our study, one tumor (T3) was POLE-mutant and three tumors (T77, T88, and T117) were microsatellite-unstable, raising the possibility that the TNK2 and DDR1 mutations in these cases may have arisen as a consequence of replicative and mismatch repair defects respectively. Here, TNK2 is linked to neoplasm.