Regarding concomitant mutations and simultaneous loss of the second EZH2 allele, the prevalence of both lesions as compared to either mutation or chromosomal loss was not as pronounced as has been described e.g. for TP53 in AML [12], where Knudson's two-hit hypothesis of sequential tumor suppressor gene inactivation fully bears out. This evidence concerns the gene EZH2 and acute myeloid leukemia.