VRL, as well as PCNSL, display typically an activated B cell-like (ABC) phenotype of diffuse large B-cell lymphoma (DLBCL), with frequent CD79B and MYD88 mutations (3, 4), which may represent a strong biological rationale for the use of BTK inhibitors in the treatment of PCNSL and VRL. This evidence concerns the gene TRPV2 and diffuse large B-cell lymphoma.