In alignment with the findings of a TCL1A-repressive impact by T-cell-derived CD40L/IL4 stimuli or by BCR signals (see Section 4.2 and Section 5.1) [12,28,84], a depleted T-cell compartment or severe EBV infection might antagonize the “B-cell developmental” (see Section 2.2) TCL1A downregulation. This evidence concerns the gene TCL1A and Epstein-Barr virus infection.