In contrast to mPIN lesions, no menin expression was detectable in the six prostate cancers found in Men1+/- mice (Figure 2C-E and 2G-I), suggesting that prostate cancer in these mice was likely caused by menin inactivation, rather than the secondary effects of MEN1 pathology, such as gene expression and/or hormone disturbance in endocrine tissues. This evidence concerns the gene MEN1 and prostate carcinoma.