APOE has also been reported to coat MSU crystals and inhibit MSU-induced inflammatory signaling [42]; therefore, the finding that urate exposure can lead to a reduction in H3K4me3 and H3K27ac (and, consequently, reduced chromatin accessibility) at the APOE locus suggests that this effect could be a point of study for the progression from hyperuricemia to gout. This evidence concerns the gene APOE and hyperuricemia.