PRDM1 and diffuse large B-cell lymphoma: Adult HGBCL, NOS cases showed distinct genomic alterations with recurrent gains at 1q, 3q27 (BCL6), chr7, 18q21 (BCL2, MATL1, TCF4), 19p and 19q13 gain (SPIB), with losses including 9p21(CDKN2A), 6q21 (PRDM1), and 17p (TP53) with similar or higher frequency to those observed in de novo ABC‐DLBCL (Figures 2B and S2), indicating that genetic aberrations target genes promoting cell‐cycle transitions, inhibiting apoptosis or are essential for B‐cell differentiation and activation.