Recent studies have found that most IP-DLBCLs harbor CD79B and MYD88 mutations, while these mutations are uncommon in LN-DLBCLs, PG-DLBCLs and PI-DLBCLs, which result in abnormal B cell receptor (BCR) signaling (via CD79B mutation) and oncogenic Toll-like receptor (TLR) signaling (via MYD88 mutation) pathways and confer lymphoma cells an advantage in selective growth at immune-privileged sites [44–47]. The gene discussed is MYD88; the disease is lymphoma.