Finally, a previously sequenced AML, reported by Hou et al.,22 carried a mutation at this position (p.G728R) and at a nearby position (p.F731L), supporting the notion that homozygous or compound heterozygous mutations at the DNMT3A—DNMT3L interface are required to effectively disrupt methyltransferase activity.23 Thus, the type, location and unusual zygosity of this somatic mutation strongly suggest mutations in DNMT3A have a causal role in the etiology of thymoma. Here, DNMT3L is linked to thymoma.