Distinctive clinical associations of KMT2A rearrangements in myeloid neoplasms rather than de novo or relapsed AML also include lymphoid-to-myeloid lineage switching among B-ALL patients treated with B-cell-targeted immunotherapy (up to 60% with KMT2A rearrangements); [29] therapy-related myeloid neoplasms, in particular in patients treated with topoisomerase II inhibitors [6,30]; and MDS/secondary AML, in which KMT2A-PTD has been described in up to 7–10% of cases [30]. This evidence concerns the gene KMT2A and myeloid neoplasm.