One of the surprises of the human genome project (Lander et al. 2001) was that only a relatively small proportion of the genome is protein coding (current estimates are around 1.2%) (Pruitt et al. 2009). The remainder of the sequence contains many repetitive sequences and transposon remnants, although a further 3–10% of the human genome displays evidence of evolutionary conservation, implying its functionality (Lunter et al. 2006). There is clearly a role for at least a proportion of this non-coding sequence in regulation of gene expression. In fact, more than 95% of disease-associated single nucleotide polymorphisms (SNPs) lie within the non-coding genome (Maurano et al. 2012). Importantly, such SNPs may be functionally relevant, since they are enriched within enhancer regions (marked by DNAse hypersensitivity) specific for the disease-associated tissue (Maurano et al. 2012), and are often associated with changes in neighbouring gene expression (Degner et al. 2012). It is also beginning to become apparent that such non-coding changes can result in phenotypic effects, and be causative in certain diseases (Soldner et al. 2016). In the context of disease modelling, such
