Mitochondria are essential organelles found in every eukaryotic cell, required to convert food into usable energy. Themitochondrial oxidative phosphorylation (OXPHOS) system, which produces the majority of cellular energy in the form ofATP, is controlled by two distinct genomes: the nuclear and the mitochondrial genome (mtDNA). Mutations in mitochondrialgenes encoded by either genome could cause diseases affecting OXPHOS system, called mitochondrial diseases, whoseprevalence has been estimated to be ≈1:8500. Moreover, dysfunction of mitochondrial OXPHOS system has emerged as akey factor in a myriad of “common” diseases, including neurodegenerative and metabolic disorders like Parkinson’s andAlzheimer’s Disease, Type 2 Diabetes, and was linked to aging process. Despite all this, it is surprising that ourunderstanding of the mechanisms governing the mitochondrial gene expression and its associated pathologies remainsuperficial and therapeutic interventions unexplored. The basic machineries for mtDNA replication, mtDNA transcription andmitochondrial translation are known, but the regulation of these processes in response to metabolic demands is poorlyunderstood. The complex nature of mitochondrial gene expression that relies on two different genomes calls for amultidisciplinary approach where different teams of researchers join forces. Studies in this area are not only of basicscientific interest but may also provide new avenues towards treatment of mitochondrial dysfunction in a variety of humandiseases.The key aim of the REMIX Network is combine the skills of European research groups to provide strategic training of thenext generation of scientists through a programme that will progress in the elucidation of the molecular mechanisms andpathways that regulate mitochondrial gene expression.