FOXC2 and breast cancer: Finally, these findings were supported by ATAC-seq, unveiling genome-wide open chromatin accessibility at TCF7, FOXC2, and FOXM1 motifs in E/M cells relative to M cells, which was reversed by ERK/CDK4/6 drug inhibition and was accompanied by suppression of mammary tumour growth and organoid formation in vitro and ex vivo.