In addition, emerging evidence shows that IRF-4 activates the CIITA pIII promoter [19], which is involved in the associated pathogenesis linked to EBV-mediated transformation of B lymphocytes, cell growth of multiple myeloma cells [20], [21], as well as acting as a tumor suppressor in early B cell development [22], all of which supports the targeting of IRF-4 by viruses for immune suppression. The gene discussed is IRF4; the disease is AL amyloidosis.