The pathophysiological process of PCNSL involves numerous distinct genetic mutations, the most important of which are functional mutations in the genes encoding the CD79b molecule (CD79B), a subunit of the B-cell receptor (BCR), and the MYD88 innate immune signal transduction adaptor (MYD88), which is involved in Toll-like receptor (TLR) and interleukin receptor signaling (3). This evidence concerns the gene MYD88 and primary central nervous system lymphoma.