If a transcription factor primarily functions downstream of Brca1 controlling EMT in breast cancers, genetically loss of or gain of function of this transcription factor in mice with the same genetic background should produce similar EMT phenotype with Brca1 deficient mice, and restoration or removal of the function of the transcription factor should eliminate Brca1 deficient EMT phenotype in mammary tumors, in addition to the regulation of the transcription factor by BRCA1 in vitro. Here, BRCA1 is linked to breast cancer.