Since PRDM14 is regulated by Wnt signaling in mouse ES cells [18,19], we validated that the therapeutic effects of silencing PRDM14 were indeed due to PRDM14 deletion in mammary tumor virus (MMTV)-Wnt-1 mice, which ectopically express Wnt and have a high incidence of spontaneous mammary adenocarcinomas containing CSC fractions [20, 21]. This evidence concerns the gene PRDM14 and breast adenocarcinoma.