Examination of the relative expression of AKT1and AKT2in these murine tissues revealed that the thyroid gland was the only tissue where AKT2 expression was higher than that of AKT1, suggesting a model whereby the onset of PTEN-deficient cancer is preferentially driven by AKT1, except in tissues where AKT2-enrichment is sufficient to co-operatively drive neoplasia. The gene discussed is PTEN; the disease is neoplasm.