In AML, 3q26.2 rearrangements targeting the MECOM locus typically abrogate expression of both the long MDS1-EVI1 isoform and, coincidentally, expression of other key myeloid regulators, such as GATA2 or MYC, while transcription of EVI1 becomes excessively increased [15–18]. The gene discussed is MECOM; the disease is acute myeloid leukemia.