Thus, aberrations most characteristic of the activated B-cell like (ABC) DLBCL subtype, which has a poor clinical outcome, include trisomy 3, gains of 3q and 18q21–q22, and deletions of 6q21–q22 and the INK4a/ARF locus on chromosome 9, whereas the germinal center B-cell (GCB) subtype, which is more common in younger adult DLBCL cases and has a better clinical outcome, exhibit frequent amplifications of 12q12, the MIHG1 locus on chromosome 13, the REL locus on chromosome 2 and deletion of PTEN on chromosome 10 [9]–[10]. This evidence concerns the gene MIR17HG and diffuse large B-cell lymphoma.