Treatment of TNBCs with AR agonists, especially accompanied by VDR agonists, leads to G1 phase arrest, increase of apoptosis, reduction of tumorsphere formation efficiency and cancer stem cell features (by deactivation of CD49f, SOX2, and Notch pathways), with epithelial transformation (increase of claudin-4, cytokeratin 18, down-regulation of cytokeratin 5 and vimentin) [134]. This evidence concerns the gene ITGA6 and cancer.