In summary, our study describes a non-enzymatic function of JMJD1C in AML, as well as an underlying mechanism that involves a direct interaction with RUNX1 and a self-interaction property that leads to formation of a JMJD1C- and RUNX1-containing condensate and long-range genomic interactions that regulate gene expression. Here, RUNX1 is linked to acute myeloid leukemia.