First, chromatin landscapes vary considerably between cell types and are highly dynamic, capable of altering in response to internal and external environmental stimuli. Given the spacial, temporal, environmental and epigenetic complexity of gene regulation, it is essential that the appropriate human cell type or model is utilized when trying to draw inferences between risk alleles and enhancer elements. Integrating risk variants with the chromatin landscapes of cell types or conditions that are insufficient models for a disorder will likely give misleading results. This is highlighted by eQTL studies. Even in comparisons of relatively similar cell types (monocytes and T cells [72] or B cells and monocytes [71]), noncoding variants that impact expression in one cell type often had no effect in the other cell type. Additionally, in a study of cis-regulation in colon cancer, the impact of some SNPs on expression was seen amongst colon cancer samples, but not observed in normal colon from the same patients, implying that the impact of the variant is dependent on disease-specific environmental factors [80]. The effect of noncoding variants on expression was also
