First, homozygous loss of exons 3–8 of the Men1 gene (Men1−/−) causes embryonic lethality in mice, while mice with heterozygous loss of Men1 (Men1+/−) develop features similar to those of the human disorder MEN1 syndrome, including increased insulin levels and decreased blood glucose levels [5, 6, 27]. This evidence concerns the gene MEN1 and multiple endocrine neoplasia type 1.