Thus, to test the effect of Shp1 loss on tumor growth, we generated a model for global, inducible deletion of Ptpn6. To achieve this, we crossed the Ptpn6fl/fl mice (25) to the Rosa26Cre/ERT2 strain (37): with this model (referred to as Ptpn6fl/flERT2-Cre), the Cre was sequestered in the cytosol by virtue of its fusion with the estrogen receptor (ER), and could only translocate to the nucleus and recombine out the loxP-flanked Ptpn6 DNA upon administration of the ER ligand tamoxifen (49). The gene discussed is ESR1; the disease is neoplasm.