Of note, lesions targeting known negative regulators of proximal BCR signaling (e.g., LYN, PTPN6, and PRKCD, among others) can be found in all DLBCL genetic subtypes, suggesting a pervasive role of BCR signaling in lymphomagenesis, through different modes of activation (“chronic, active” vs. “tonic”, or antigen-independent) and distinct downstream signaling cascades (NF-κB vs. PI3K). Here, NFKB1 is linked to diffuse large B-cell lymphoma.