However, cases with KMT2A (lysine methyltransferase 2A) and NUP98 (nucleoporin 98) rearrangements now form independent subgroups of AML with defining genetic abnormalities (that also include other non-AMKL phenotypes), and cases with CBFA2T3 (CBFA2/RUNX1 partner transcriptional co-repressor 3)::GLIS2 (GLIS family zinc finger 2) and RBM15 (RNA binding motif protein 15)::MKL1 (megakaryoblastic leukemia 1) fusions belong to a subgroup of AML with other defined genetic alterations. This evidence concerns the gene GLI2 and acute myeloid leukemia.