Consequently, dysregulated IL-6/STAT3/BCL6 signaling—further amplified by EBV-induced inflammation—may represent a biological link between AITL and coexisting plasma-cell neoplasms, providing a rationale for the emergence of plasma-cell clones both within AITL lesions and in the bone marrow compartment. Here, STAT3 is linked to angioimmunoblastic T-cell lymphoma.