The distinction between duodenal gastrinomas/somatostatinomas and hyperplastic lesions is explained by the fact that a loss of heterozygosity (LOH) of MEN1 and/or centromere 11 was demonstrated in approximately 50% of MEN1-associated duodenal NETs; however, hyperplasia or precursor lesions consistently lacked LOH on chromosome 11q13 (18). Here, MEN1 is linked to duodenal gastrin-producing neuroendocrine tumor.