Abstract
Neurofibromatosis type 1 (NF1) is the most common (0.03%) autosomal dominant inherited disorder.1 In NF1, neurogenic and carcinoid tumors occur as a result of transformation of an endodermal-ectodermal complex that is present near the ampulla of Vater. The mutation of the NF1 gene (17q11.2) is responsible for NF1 disease. This gene encodes for neurofibromin, a guanosine triphosphatase protein involved as a negative regulator of the Ras pathway and in particular of mammalian target of rapamycin function, whose overactivation may be a key event in neuroendocrine tumor development in this area.
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