Maternally expressed gene 3 ( ) is a long noncoding RNA (lncRNA) that has been implicated as a tumor suppressor. The expression of RNA is downregulated in various human tumors, including pituitary adenoma and pancreatic islet tumors due to gene deletion or DNA hypermethylation. Mouse models with conventional germline deletion of have shown that is essential for perinatal or postnatal development and survival. However, a direct role of loss in tumorigenesis has not been shown. To observe a causal relationship between loss and tumorigenesis, we have generated a mouse model with conditional deletion of mediated by the RIP-Cre transgene that initiated deletion in pancreatic islet β cells and anterior pituitary. loss did not lead to the development of islet tumors. Interestingly, RIP-Cre-mediated loss led to the development of an enlarged pituitary. The genes in the region are transcribed together as a 210 kb RNA that is processed into and other transcripts. Whether these tandem transcripts play a functional role in the growth of pancreatic endocrine cells and pituitary cells remains to be determined. Our mouse model shows that loss leads to hyperplasia in the pituitary and not in pancreatic islets, thus serving as a valuable model to study pathways associated with pituitary cell proliferation and function. Future mouse models with specific inactivation of alone or other transcripts in the polycistron are warranted to study tissue-specific effects on initiating neoplasia and tumor development.