Imbalanced expression of MECOM-transcribed isoforms is often the consequence of (i) chromosomal rearrangements leading either to EVI1 gene fusions (e.g., AML1-EVI1) [12]; (ii) MECOM locus amplifications as found with high frequency in high-grade serous ovarian cancer [13]; (iii) aberrant promoter activation [14]; or (iv) displacement of regulatory DNA elements into the EVI1 locus, the latter being a hallmark of 3q26.2/MECOM rearranged acute myeloid leukemia (AML) [15, 16]. Here, RUNX1 is linked to ovarian serous adenocarcinoma.