Mutations in the breast cancer susceptibility gene, BRCA1 confer an increased risk of developing breast cancer. Although the cellular and pathological consequences of BRCA1 disruption are well documented, the early molecular consequences associated with these are not well characterized. Studies conducted on conditional Brca1 knockout mice, have revealed that they exhibit aberrant mammary gland morphogenesis and develop tumours with a similar histological and gene expression profile to human BRCA1 associated breast tumours. This makes the conditional Brca1 knockout mouse an excellent model to study molecular mechanisms of BRCA1 associated breast cancers. miRNAs play a role in the development and homeostatic regulation of the mammary gland and tumourigenesis can occur if miRNAs are abnormally expressed. To investigate the role of miRNAs, a candidate approach was undertaken to shortlist miRNAs with known roles in breast cancer and mouse mammary gland development. The expression of the shortlisted miRNAs was assessed in Brca1 deficient mice mammary tissue and the HC11 mammary epithelial cell line. miR-206 was up-regulated in Brca1 deficiency. The up-regulation of miR-206 impaired HC11 mammary epithelial differentiative capacity. Furthermore miR-206 was shown to functionally target Sfrp1, hereby potentially contributing to the effects of Brca1 dysfunction in the mammary gland. Recent findings from miR-206 over-expressing mice mammary glands are indicative of a potential mammary epithelial degenerative defect which is currently being followed up upon. Given that the uses of miRNAs are currently being trialed in the field of cancer, these studies may have therapeutic implications in the treatment of BRCA1 associated breast cancers.