Furthermore, genetic analyses revealed that TFB1M is a type 2 diabetes risk gene and consistent with this, a TFB1M+/− mouse model showed impaired mitochondrial translation in pancreatic islet cells and reduced insulin production in response to glucose, implying that lack of 12S modification and the consequent mitochondrial dysfunction contribute to the pathogenesis of type 2 diabetes [42, 43]. This evidence concerns the gene INS and type 2 diabetes mellitus.