Hypermethylation of promoters of tumor suppressor genes, following menin loss, was demonstrated to be a common pro-oncogenic epigenetic change in MEN1 pancreatic neuroendocrine tumors [11], and a similar mechanism can be suspected also in MEN1 loss-driven parathyroid tumorigenesis, both for the syndromic and the sporadic forms. Here, MEN1 is linked to pancreatic neuroendocrine tumor.