Besides disease-related changes in the heart structure and function, there are also congenital genetic changes that cause heart failure. These can be treated by classical gene therapy, in which the defective protein is replaced by a correct one. However, this approach is limited by the size of the protein to be replaced. Novel therapeutic approaches therefore aim at directly for correcting the defective sequence of the protein formed (in vivo genome editing). Our group is pursuing approaches in which adeno-associated viral vectors transport recombinases (enzymes) into the affected cells, which are capable to repair the gene sequences.