Given that even a slight reduction in PTEN levels can significantly increase tumor formation [20,60], the ability of PRL2 to down-regulate PTEN, through both a miR-21-dependent post-transcriptional mechanism and the previously reported NEDD4-dependent post-translational PTEN regulation [19], contributes to its oncogenic potential to enhance cancer progression. The gene discussed is PTP4A2; the disease is cancer.