Prof. Manolis Mavroidis received his Ph.D. in Molecular Biology in 1997 from the University of Patras, Greece. He worked as a research specialist at the University of Pennsylvania, USA, where he studied the complement system, and then as a postdoctoral fellow at the Baylor College of Medicine, Houston, USA (1999–2002), studying the role of the intermediate filament cytoskeleton in cardiomyopathy and heart failure development. Currently, Dr. Mavroidis is an investigator at the Biomedical Research Foundation Academy of Athens. Dr. Mavroidis’s laboratory is focused on fundamental pathogenetic mechanisms underlying dilated (DCM) and arrhythmogenic cardiomyopathy (ACM), using transgenic mice models with mutations in cytoskeletal proteins (desmin, dysferlin and ankyrin 6) identified in human patients suffering from DCM or ACM; in combination with mice models with the depletion of innate immunity and metabolism-related genes, such as C3, C5a receptor and C5L2 receptor. His studies were the first to implicate complement system activation in the progression of ACM (doi: 10.1007/s00395-015-0485-6). Also, recently, he showed that crosstalk between the complement and coagulation systems exacerbated myocardial injury in ACM (doi: 10.7150/thno.58160), suggesting a promising translational perspective. His research is motivated by the hope of discovering new therapeutical targets and tools for diagnosing and treating DCM/ACM.