These phenotypes are linked, in that the natural history of MPN, CML and MDS leads to transformation to AML in a proportion of cases and that they share a number of common mutations, particularly those altering epigenetic regulators such as the DNA methyltransferase 3A (DNMT3A), the DNA‐demethylase TET2 and the BAP1‐interacting factor ASXL1 [1]. This evidence concerns the gene DNMT3A and acute myeloid leukemia.