Wolfram syndrome, characterized by early-onset diabetes, optic atrophy, deafness, and diabetes insipidus is due to mutations of the WFS1 gene [34], which regulates ί cell function in mice [35] and glucagon-like peptide 1-induced insulin secretion in humans [36], suggesting that impaired beta cell function in subjects with the risk allele of WFS1 may promote the onset of T2D as seen in other monogenetic diabetes [37,38]. Here, WFS1 is linked to hereditary optic atrophy.