Double transgenic mice obtained crossing heterozygote Drp1 (+/−) mice with AD mice (Tg2576 strain) reveals that partial reduction of Drp1 is beneficial by ameliorating mitochondrial dysfunction, reducing Aβ production, increasing mitochondrial biogenesis and enhancing synaptic activity (Manczak et al., 2016). The gene discussed is DNM1L; the disease is Alzheimer disease.