These mice overexpress Bcl2 in the hematopoietic system, leading to a predisposition to suffer from follicular lymphoma and subsequently premature death.2 It has been shown that the overexpression of a transmembrane activator and a CAML interactor receptor, coupled to the Fc-fragment of human immunoglobulin G (TACI-Ig) (causing the neutralization of the survival and maturation factor for B-cells, BAFF (B-cell activating factor of the TNF family)) is able to decrease the number of B-cells in Vav-Bcl2 mice, which alleviates disease burden and subsequently prolongs the survival of these mice. This evidence concerns the gene VAV1 and follicular lymphoma.