Interestingly, wild-type USP2 was not transcribed in majority of B-ALL patients (Figure 4A) and could be activated through fusion with KMT2A (Figure 4B), with active transcription of USP2 occurring through hijacking of the KMT2A promoter (Supplementary Figure 3). This evidence concerns the gene KMT2A and precursor B-cell acute lymphoblastic leukemia.