Moreover, the feedback loop linking DYRK1A inhibition to modulation of the main mitochondrial protein biogenesis pathways may also help to elucidate the molecular mechanisms underlying the clinical manifestations of DYRK1A syndrome: Patients with dysfunctional DYRK1A present with symptoms such as motor deficits, microcephaly, speech delay, intellectual disability and autism, which, especially in their combinations, resemble typical mitochondrial disease phenotypes22,64–69. The gene discussed is DYRK1A; the disease is inborn mitochondrial metabolism disorder.