This phenotype is surprising given that mouse fibroblasts derived from Dync1h1+/Cra1 and Dync1h1Cra/Cra1 embryos display profound alterations of mitochondrial morphology and that Dync1h1+/Cra1 mice develop, hyperinsulinemia, hyperglycaemia, and progressive mitochondrial dysfunction [58]. This evidence concerns the gene DYNC1H1 and hyperinsulinism.