In melanoma withBRAFmutation, the upregulated H3K9Me3 level was reported to be associated with increased treatment resistance.42Moreover, H3K9Me3, as well as its associated methylation enzymes (SUV39H2 and SETDB1), was shown to regulate gene expression in the hedgehog and Wnt/B-catenin signaling pathways.22, 44Since these genetic alterations are also detected in odontogenic lesions, including ameloblastoma, AOT, and OKC, it is likely that these crosstalks between genetic and epigenetic mechanisms exist and deserve further investigation. This evidence concerns the gene SETDB1 and ameloblastoma.