Bmi1 facilitates the repression of Hox genes to prevent inappropriate differentiation and induces downregulation of Dickopf (DKK) proteins, resulting in upregulation of the Wnt target c-Myc, which in turn leads to transcriptional autoactivation of Bmi1. 7 Reinforcement of this positive feedback loop regulating Bmi1 expression seems relevant in promoting cancer and maintaining the stem cell phenotype.9, 10 In addition, Bmi1 is transcriptionally controlled by phosphorylated Nanog,11, 12 and is inhibited by a plethora of miRNAs that are significantly downregulated in cancer models.12 This evidence concerns the gene NANOG and cancer.