In vivo models of GEP-NET pathogenesis are historically lacking, in part due to tissue heterogeneity from which neoplasms arise, and the absence of known driver mutations preceding malignancy.131 Nevertheless, the 21st century has seen an expansion in the number of transgenic mouse models aimed at clarifying the role of MEN1 and other putative drivers in GEP-NET emergence.132–134 Francis Collin's group at the National Human Genome Research Institute was among the first to recapitulate the human MEN1 syndrome through homologous recombination of the Men1 locus. Here, MEN1 is linked to neoplasm.