Alternatively, the DNMT3L:DNMT3A interface is disrupted by somatic mutations within the mutational hotspot region centered on the p.G728D mutation observed in this thymoma.23 Heterozygous mutations at this site may not be expected to influence activity as markedly as mutations at p.R882 as they likely allow for the formation of partially complete complexes, for example, DNMT3A:DNMT3A:DNMT3L complexes could form 50% of the time. The gene discussed is DNMT3A; the disease is thymoma.