In addition, POLD1 has also been shown to have critical roles in proofreading by DNA polymerases.3 Previously, rare germline mutations in POLE and POLD1 have been reported in patients with polymerase proofreading‐associated polyposis,23, 24 suggesting that germline POLE and POLD1 mutations were involved in familial CRCs.25 However, it is still unclear whether somatic POLD1 mutations act as drivers of spontaneous CRCs.7 In this study, although some tumors harbored the exonuclease domain of POLD1 (data not shown), we did not examine whether these mutations were pathogenic. The gene discussed is POLE; the disease is polyposis.