Given that the composition and morphology of myeloid populations of the PRL2-KO;PTEN HET animals more closely resembled that of the WT and PRL2-KO animals at 40 weeks — but, in the longer term (>60 weeks), exhibited AML characteristics — the mechanism by which PTEN restoration through PRL2 deletion improves survival appeared not to be by preventing the formation of LSCs but rather by reducing the rate of HSC to LSC transition and the accumulation of LSC-derived leukemia blasts that progressed the AML phenotype. The gene discussed is PTEN; the disease is leukemia.