In KMT2A-MLLT3 cells, loss of menin specifically reduces the expression of genes that are upregulated by the fusion protein, but KMT2A deletion did not have the same effect on these genes.28,29 Therefore, although menin is associated with both endogenous KMT2A and KMT2A-FPs, it appears to only be required for the function of the fusion protein in the context of AML. Here, MLLT3 is linked to acute myeloid leukemia.