Since the lack of CD69 expression in the Vav1–/–;Rasgrf2–/– tumor cells suggests that their growth is mediated by TCR–independent mechanisms, the synergistic interaction between the Vav1 and Rasgrf2 gene deficiencies will probably need the alteration of TCR–independent routes rather than the canonical TCR downstream pathways for this hypothesis to be correct. This evidence concerns the gene RASGRF2 and neoplasm.