PRDM14 and cancer: Our previous aCGH data of PRDM14-induced pre-B and pre-T ALLs found a large number of common deletions and amplifications in pre-B-cell and mixed lineage cell tumors, yet pre-T-cell tumors were relatively free of common copy number variants with the exception of those at Notch1. Common genomic rearrangements in pre-B-cell and mixed lineage tumors occurred at sites bound by PRDM14, many of which contain cRSSs, including cyclin dependent kinase 2a (Cdkn2a), a common driver in cancers (Simko et al., 2012).