At the same time, the epigenetic silencing of wild type menin by miR-24 promotes cell proliferation and exposes cells to DNA damage, which could result in deletion at the 11q13 locus or mutation of the second copy of the MEN1 gene, favoring the somatic MEN1 LOH, which represents a common hallmark of MEN1 cancers in parathyroids and endocrine pancreas. The gene discussed is MEN1; the disease is cancer.