In AML and ALL, overexpression of the miR-17-92 cluster is caused by either copy number amplification or direct targeting by MLL fusions, leading to increased cell proliferation and inhibition of apoptosis, suggesting that miR-17-92 may play a role in the development of MLL-rearranged leukaemia [186]. This evidence concerns the gene KMT2A and acute lymphoblastic leukemia.