The HR signature in POLE mutants was high in comparison with that in common hypermutator tumours (p = 6.06 × 10−5, Fig. 4a), whereas mutations of HR-/NHEJ-related genes20,21 were accumulated in POLE-category tumours (Fig. 4b), implying that HR activity in tumours harbouring defective POLE were elevated despite mutation accumulation in HR genes. This evidence concerns the gene POLE and neoplasm.