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]. The gene discussed is KRT18; the disease is cancer.