Furthermore, the use of catalytically deficient Vav2 knock-in mice has demonstrated that the inhibition of the enzymatic activity of Vav2 impairs both the papilloma and cSCC formation that are typically induced upon the topic administration of the carcinogen 7,12-dimethylbenz(a)anthracene (DMBA) either alone or in combination with the tumor promoter 12-O-tetradecanoylphorbol-13-acetate (TPA)11. Here, VAV2 is linked to neoplasm.