However, ectopic expression of OCT4 in the intestinal epithelium and epidermis blocks differentiation and leads to uncontrolled proliferation of progenitor cells (Hochedlinger et al., 2005), and forced overexpression of OCT4 in primary breast epithelial cells generated tumor-initiating cells (Beltran et al., 2011), suggesting that reactivation of epigenetically silenced OCT4 would be a parsimonious route to tumor formation. This evidence concerns the gene POU5F1 and neoplasm.