This rate is seven times higher than that observed in DDD, and was attributed to a potential RT mutation hotspot associated with the canonical L1 endonuclease cleavage site of 3′-AA/TTTT-5′38 within the neurofibromatosis-associated gene, NF1. A recent study using a cell culture retrotransposition assay to study MEI site preference was unable to identify a mutation hotspot in NF139, and therefore suggests further work is needed to investigate the role of sequence context in determining the overall genomic landscape of RT-mediated disease. This evidence concerns the gene NF1 and neurofibromatosis.