The evolutionary conservation of mammalian genomes, especially in protein coding sequence, has enabled the use of many animal models such as mice, rats and non-human primates for studying the effects of genetic lesions upon molecular, cellular, physiological and behavioural phenotypes. This has led to many important insights into disease biology, and their importance in such studies is undeniable. Despite such conservation of function, given the last common ancestor of human and mouse was around 100 million years ago (Mouse Genome Sequencing Consortium et al. 2002), it is unsurprising that there are also differences between these organisms. Around 20% of genes in humans lack an identifiable one-to-one orthologue in mouse (Mouse Genome Sequencing Consortium et al. 2002), and the number of paralogs within an organism is often different, many of which have diverged to provide subtly different functions (Gabaldon and Koonin 2013). Equally, even apparently orthologous genes can play different roles, such as in the case of TDP1, which shows a different subcellular localisation in humans and mice, and mutations in which are linked to the SCAN1 disorder in humans, but
