The conservative nature of gene deserts confirms that these stretches of noncoding bases are essential to proper functioning. Indeed, a wide range of studies on irregularities in the noncoding genes discovered several associations to genetic diseases. One of the most studied gene deserts is the 8q24 region. Early genome wide association studies were focused on the 8q24 region (residing on chromosome 8) due to the abnormally high rates of SNPs that seem to occur in the region. These studies found that the region was linked to increased risks for a variety of cancers, notably in the prostate, breast, ovaries, colonic, and pancreas. Using inserts of the gene desert into bacterial artificial chromosomes, one study was able to produce enhancer activity in certain regions, which were isolated via cloning systems. This study successfully identified an enhancer sequence hidden in the region. Within this enhancer sequence, an SNP that conferred risk for prostate cancer, labeled SNP s6983267, was discovered in diseased mice. However, the 8q24 region is not solely limited to conferred risks of prostate cancer. A study in 2008 screened human subjects (and controls) with variations in the gene desert region, discovering five different regions that conferred different risks when affected by different SNPs. This study used identified SNP markers in the gene desert to identify risk conference from each of the regions to a specific tissue expression. Although these risks were successfully linked to various forms of cancer, Ghoussaini, M., et al. note their uncertainty in whether the SNPs functioned merely as markers or were the direct causants of the cancers.
These varied effects occur due to the different interactions between the SNPs in this region and MYC promoters of different organs. The MYC promoter, which is located at a short distance downstream of the 8q24 region, is perhaps the most studied oncogene due to its association with a myriad of diseases. Normal functioning of the MYC promoter ensures that cells divide regularly. The study postulates that the 8q region, which underwent a chromosomal translocation in humans, could have moved an essential enhancer for the MYC promoter.  This areas around this region could have been subjected to recombination that may have hidden the essential MYC enhancer within the gene desert through time, although its enhancing effects are still very much retained. This analysis stems from disease associations observed in several mice species where this region is retained at proximity to the MYC promoter. Thus, the 8q24 gene desert should have been somewhat linked to the MYC promoter. The desert resembles a stable gene desert that has had very little recombination after the translocation event. Thus, a potential hypothesis is that SNPs affecting this region disrupt the important tissue-specific genes with the stable gene desert, which could explain the risks of cancer in various tissue forms. This effect of hidden enhancer elements can also be observed in other locations in the genome. For instance, SNPs in the 5p13.1 deregulate the PTGER4 coding region, leading to Crohn's Disease. Another affected region in the 9p21 gene desert causes several coronary artery diseases. However, none of these risk-conferring gene deserts seem to be affected as much as the 8q24 regions. Current studies are still unsure about the SNP-affected processes in the 8q24 region that result in particularly amplified responses to the MYC promoter. With the aid of a more accessible population and more specific markers for genome wide association mapping, an increasing number of risk alleles are now being marked in gene deserts, where small, isolated, and seemingly-unimportant regions of genes may moderate important genes.