In summary, we propose that upon SNAI1 knockout, TNBC-basal cells are reprogrammed to the hybrid epithelio-mesenchymal phenotype of the EMT spectrum, while further generating basal-luminal plasticity as indicated by re-expression of FOXA1 and AR, and by shifting the differentiation balance towards a more proliferative and less invasive breast cancer cell population (Fig. 7J, Supplementary Fig. 7). The gene discussed is SNAI1; the disease is breast carcinoma.