Given this, in order to determine the role of endogenous Dach1 in mediating prostate transformation, multigenic mice were generated by crossing conditional Dach1 gene deletion mice [33] with prostate-specific Cre transgenics, using Probasin-Cre4 (Pb-Cre4) transgenic mice, which express Cre in both the basal and luminal prostatic epithelia, then further intercrossing with the TRAMP model of prostate cancer (Fig. 3A). The gene discussed is DACH1; the disease is prostate cancer.