Results suggest that highly proliferative testicular lymphoma cells with enhanced cell cycle, elevated genomic stress, activated BCR signaling, and likely immune escape mechanisms are drivers of aggressive PT-DLBCL and confer poor clinical outcome; in contrast, the unique TME in PT-DLBCL harbors antitumor factors conferring better prognosis, especially in younger patients. This evidence concerns the gene BCR and diffuse large B-cell lymphoma.