In the case of type-2 tumors, in patients with MEN-1, a hereditary condition caused by mutations which inactivate the tumor suppressor gene MEN1, the tumorigenic influence of gastrin may be accentuated by reduced tumor suppression, an additional factor in inducing carcinoids [16], although it must also be pointed out that despite the fact that using villin-Cre to delete the MEN1 locus in the gastrointestinal epithelium generated hypergastrinemia, G-cell hyperplasia and epithelial dysplasia, no ECL tumors developed [17]. This evidence concerns the gene GAST and multiple endocrine neoplasia type 1.