In summary, future in-depth analysis of biomolecular condensates induced by NPM1c, NUP98-, and/or KMT2A-fusion proteins and other AML oncoproteins may allow to dissect not only novel critical protein-protein interactions but also transcription-permissive gene loci that are prevalent in preleukemic clones and might be associated with a higher risk for progressing toward AML. The gene discussed is KMT2A; the disease is acute myeloid leukemia.