This high frequency of CHEK2 variants in pure DCIS has not been previously described, although Schmidt et al. noted in their study of tumour characteristics in CHEK2 c.1100delC carriers that carriers from population- and hospital-based studies more often developed in situ tumours (LCIS and DCIS) compared to carriers from familial or clinical genetics center–based studies; this was interpreted as a bias estimate due to differential recruitment related to family history of breast cancer and screening [26]. This evidence concerns the gene CHEK2 and breast carcinoma.