Taking a more systematic approach to the capsid protein-engineering problem, researchers mutated one by one each of the 735 amino acids within the AAV2 capsid, the best-known member of the AAV family, including all possible codon substitutions, insertions and deletions at each position. They generated a virus library containing about 200,000 variants and identified capsid changes that both maintained AAV2’s viability and improved its ‘homing’ potential (tropism) to specific organs in mice.