The downregulation of Oct4 via PRPc suppression may be explained by a cancer-specific mode of Oct4 upregulation, in which the interacting factors PRPc and c-MET (c-mesenchymal–epithelial transition), the latter being a (proto-)oncogen frequently found in tumor cells, jointly upregulate ERK1/2, which stimulates Oct4 expression [240]. The gene discussed is POU5F1; the disease is cancer.