Molecular features often found in PCNSL are TLR and B cell receptors (BCR), signalling coactivation through MYD88 and CD79B mutations, with the activation of the NF-κB pathway and homozygous losses of CDKN2A, leading to genomic instability and mechanisms of immune escape, namely the loss of the HLA locus on 6p21.33 and PD-L1/2 overexpression [46,47]. Here, MYD88 is linked to primary central nervous system lymphoma.