Briefly, the “chronic” BCR signaling in ABC-DLBCL is characterized by the many pathways involved with the CARD11-mediated activation of NF-κB signaling, whereas the “tonic” BCR signaling in GCB-DLBCL is characterized by the constitutive activation of PI3K in promoting survival [96, 97]. This evidence concerns the gene PIK3CA and aneurysmal bone cyst.