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To understand their pathogenic potential, we generated a gene\u2010edited mouse model that expresses a VAV1 mutant protein that recapitulates the signalling alterations present in the\n                    <jats:italic>VAV1<\/jats:italic>\n                    mutant subclass most frequently found in tumours. We could not detect any overt tumourigenic process in those mice. However, the concurrent elimination of the\n                    <jats:italic>Trp53<\/jats:italic>\n                    tumour suppressor gene in them drives T cell lymphomagenesis. This process represents an exacerbation of the normal functions that wild\u2010type VAV1 plays in follicular helper T cells. We also found that, in combination with the\n                    <jats:italic>Kras<\/jats:italic>\n                    oncogene, the VAV1 mutant version favours progression of NSCLC. 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