Given the high prevalence of MYD88 mutations in primary CNS A-DLBCL, treatment with ibrutinib, which inhibits Bruton’s Tyrosine Kinase (BTK) and further suppresses NF-κB and STAT3 activation and tumor growth, or treatment with bortezomib, which is effective for CD79B/MYD88L265P double-mutant DLBCLs [33], could be considered in patients with primary CNS A-DLBCL [34]. The gene discussed is STAT3; the disease is neoplasm.