The fact that genes such as the MHC genes that are under balancing selection in type I genes may be due to their requirement for ongoing variation as copy number variation is another method of increasing the potential for variation amongst individuals. The type III genes are under very different evolutionary pressures than type I genes as they have evolved long UTRs and are significantly enriched for genes that are regulated by miRNAs. Their lower mutation rates mean that miRNA targets are less likely to be high content screening disrupted by point mutation. There is the possibility that the CNV itself might disrupt the UTR but most CNV breakpoints in type III genes are within the introns and are often associated with repetitive elements such as Alu, so the CNV is unlikely to disrupt the 39UTR and it’s miRNA targets. Also, CNVs that completely overlap the 39UTR will be classified as type Life Science Reagents genes. The type III genes are significantly enriched for genes that are normally monoallelically expressed. Initially this result was rather surprising but recent work linking monoallelic expression with recombinant hotspots may help to explain this significant enrichment. Necsulea et al. hypothesised that the differential methylation status of the silenced and active alleles of the monoallelically expressed genes may somehow be responsible for the increased recombinant hotspots in these genes. This begs the question whether the same mechanisms may be responsible for these recombinant hotspots as well as the CNV breakpoints? The gene functional annotation clustering highlighted that many type III genes produce proteins that contain extracellular domains which agrees with Gimelbrant et al. who found many monoallelically expressed genes were involved in cell to cell signalling. These domains are known to have evolved through the evolutionary process of exon shuffling where whole exons and domains are duplicated or deleted within a gene. It is interesting that this mechanism is currently in action in the human genome. Unlike type I genes, type III genes appear to be regulated by a number of potential dosage compensation mechanisms despite being present in just the wild type copy number.