MEN1 and neoplasm: These altered epigenetic mechanisms (loss of H3K4me3 and gain of H3K27me3), subsequent to menin absence/reduction, which appear to drive the MEN1-associated beta cell tumorigenesis, can be reversed by inhibiting/silencing the H3K4me3 demethylase Rbp2, suggesting this enzyme as a possible target of an early-stage epigenetic therapy for tumors of the beta cells in MEN1 patients [27].