Acinetobacter baumannii is an ESKAPE pathogen due to extensive antibiotic resistance. In most countries, strains resistant to many different antibiotics are associated with a few globally disseminated clones, and the GC1 and GC2 clones have been dominant since the late 1970s. However, many different GC1 and GC2 lineages have evolved over the decades, each derived from a single cell that acquired a novel feature and some have subsequently circulated globally. To understand and track the spread of these important clones, an understanding of the evolution of these lineages and the relationships between them is needed. We are exploring the evolution of the GC1 and GC2 clonal complexes using de-novo assemblies generated using Velvet or SPAdes of genomes sequenced using Illumina HiSeq, coupled with completed reference genomes. Resistance gene content and resistance mutations are assessed and chromosomal resistance islands are assembled using PCR. Plasmid sequences are retrieved via matches with known plasmids and complete plasmid sequences assembled. Some lineages can be defined by variations in the identity and gene content of the resistance islands, and carbapenem or aminoglycoside resistance genes have been acquired repeatedly generating a multitude of further sub-lineages. Extracellular polysaccharides, which are critical virulence factors, also vary due to extensive within clone variation in the gene content at the K (capsule biosynthesis) and OC (outer core of lipooligosaccharide) loci. Recently, locations of ISAba1 insertion sequences have been identified using ISMapper and ISSeeker and verified by PCR in a reference. The locations of shared ISAba1s correlate well with standard phylogenies, and using ISAba1 locations we have begun to deduce evolutionary pathways in the clone as a whole and within specific lineages. Specific locations of ISAba1 can be detected simply using PCR and are likely to provide highly discriminatory markers for outbreak detection and detecting international spread.