PRDM1 and precursor B-cell acute lymphoblastic leukemia: Based on our whole transcriptome sequencing, functional screening with CRISPR-cas9, response to Selinexor, the known Pre-BII to immature B cell metabolic checkpoint [47] and PRDM1 functions in transcriptional repression (reviewed in [51]), we propose a model to explain the role of 6q deletions in B-ALL (Fig. 7).