FISH confirmed the presence of the ETO/AML1 fusion signal in the intracranial lesion, suggesting homology with the primary AML (2).Molecular biological testing not only confirmed the presence of the RUNX1::RUNX1T1 fusion gene, which was identical to that in the initially diagnosed AML, but also identified truncating mutations in the MGA gene. The gene discussed is RUNX1T1; the disease is acute myeloid leukemia.