Mutations in PTEN, a tumour suppressor gene, occur at a high frequency in human cancer. The gene encodes a phosphatase that acts in signalling pathways to negatively regulate cell growth. Inactivation of PTEN leads to increased cell proliferation and reduced cell death, resulting in tumour formation. Until now, it has proven difficult to induce complete PTEN loss in different tissues simultaneously because of the protein’s crucial role in development. Here, Mirantes and colleagues describe an inducible PTEN knockout mouse model. Tamoxifen-induced PTEN deletion resulted in the rapid development of hyperplasias and neoplasias in endometrial, prostrate and thyroid tissue and administration of a known anti-tumoral drug, everolimus, hindered carcinogenesis. These data validate the model as a valuable tool for investigating PTEN-negative cancers and for testing the efficacy of new therapies. Page 710

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