Differentiation in luminal tumours is sustained by a cooperative network between the TFs ER, FOXA1 and GATA3, but little is known about how this is regulated during metastasis progression or treatment resistance, aside from some specific mutations in TFs (for example, SY242CS BCa mutation in FOXA1) or chromatin remodellers (for example, histone methyltransferases and histone demethylases)16,39,53–55. Here, GATA3 is linked to neoplasm.