The tumorigenesis in MEN-1 follows Knudson’s two-hit hypothesis, requiring both a germline heterozygous inactivating mutation in the MEN1 tumor suppressor gene and subsequent somatic loss of the remaining wild-type allele through loss of heterozygosity (LOH) in target tissues (9, 10). This evidence concerns the gene MEN1 and multiple endocrine neoplasia type 1.