More remarkably, we found that MALAT1 displayed significantly higher expression levels in the AML patient subgroups with fusion proteins, including t(11q23)/MLL, AML1-ETO, PML-RAR, and CBFb-MYH11A, than those without (Fig. 1f), indicating that it may regulate the expression of chromosomal translocated genes in a common mechanism in the aggressive AML. This evidence concerns the gene RUNX1 and acute myeloid leukemia.