A recent study reported on the role of SPIB in ABC-DLBCL using biotin-tagged SPIB for ChIP-seq assays, and concluded that SPIB/IRF4 heterodimers were central to ABC-DLBCL pathogenesis potentially regulating B-cell receptor signalling pathways and interferon-α (IFNα) secretion downstream of MYD88 mutations (16). The gene discussed is IFNA1; the disease is aneurysmal bone cyst.