We considered the possibility that decreased IRF4 expression contributes to the lytic phenotype of T2 EBV-infected LCLs since IRF4 (although essential for T1 LCL survival [39,40]) has been shown to inhibit BCR signaling [41], and decreased IRF4 expression enhances the growth of BCR-dependent chronic lymphocytic leukemia tumors in both humans and mouse models [42–45]. This evidence concerns the gene BCR and B-cell chronic lymphocytic leukemia.