In the case of t(7;12) AML (herein MNX1-r) (Ragusa et al., 2023), in which the translocation results in transformation-driving ectopic expression of MNX1 (Waraky et al., 2024), analysis of patient transcriptional signatures (Ragusa et al., 2022) for over-representation of cell atlas-defined affiliations, indicates enrichment in cardiomyogenic, endothelial, HSC/progenitor, and mast cells (Figure 5A). This evidence concerns the gene MNX1 and acute myeloid leukemia.