GPT and pancreatic insulinoma: These subgroups form as follows: the development of α like tumors from α-cells is enhanced by MEN1 mutation; tumor progression is associated with intermediate tumors gradually losing differentiation due to DAXX/ATRX mutations, chromosomal differentiation instability with recurrent LOH and ALT activation; β-like tumors develop from β-cells and usually manifest as insulinomas with indolent course and distinct genetic background [19].