Using a collection of follow-up samples from 14 patients with a primary hematologic malignancy who developed a secondary AML, our data showed that clonal evolution in t-MN is a heterogeneous process, with some somatic mutations (such as TP53 and ASXL1) preceding cytotoxic treatment and possibly favoring leukemic development [59]. Here, TP53 is linked to acute myeloid leukemia.