To understand the mechanisms that can explain the observations about RKIP and BACH1 showing opposite trends with respect to metastatic propensity, we identified a minimal core underlying GRN in breast cancer that incorporates the feedback loops that RKIP and BACH1 are involved in with key players of EMT, tamoxifen resistance and stemness, building on our previous efforts to connect these axes of plasticity [12,40]. This evidence concerns the gene BACH1 and breast carcinoma.