These transgenic mice have a tamoxifen inducible Cre-mediated recombination system driven by the mouse neurogenin 3, Neurog3, promoter. The transgene insert contains a fusion product involving Cre recombinase and a mutant form of the mouse estrogen receptor ligand binding domain. The mutant mouse estrogen receptor does not bind natural ligand at physiological concentrations but will bind the synthetic ligand, 4-hydroxytamoxifen. Restricted to the cytoplasm, the Cre/Esr1 protein can only gain access to the nuclear compartment after exposure to tamoxifen. When crossed with a strain containing a loxP site flanked sequence of interest, the offspring are useful for generating tamoxifen-induced, Cre-mediated targeted deletions. Tamoxifen administration induces Cre recombination in islet cells of the pancreas, undifferentiated spermatogonia and other Neurog3 expressing cells. Transgene expression closely patterns endogenous gene expression as analyzed by in situ hybridization. Hemizygous mutant mice are viable, fertile, normal in size and do not display any gross physical or behavioral abnormalities. The donating investigator has not attempted to make these mice homozygous. The Jackson Laboratory 2024, used with permission.