Given the inverse correlation of PRL2 overexpression and the reduction in PTEN protein level in clinical samples of AML, together with the role of PTEN in the regulation of HSC proliferation (17), an AML mouse model was generated to further investigate the regulatory role of PRL2 on PTEN protein level, PTEN-regulated pathways, and the onset and progression of the AML phenotype. The gene discussed is PTP4A2; the disease is acute myeloid leukemia.