In a different experimental system, an analysis of tumorigenesis in the immune system showed that in adoptive T cell transfer experiments, a trivalent subclass VAV1 mutant can directly induce the development of AITL in vivo [108]; this mutant is a VAV1 mutant allele that produces a CSH3-truncated protein (amino acids 835–845) and exhibits strong RAC and NFAT activity but is unable to inhibit ICN1 signaling. This evidence concerns the gene VAV1 and angioimmunoblastic T-cell lymphoma.