Although we cannot exclude the possibility that Ras1A overexpression and/or downregulation of Pten may also contribute to the observed phenotype, it is possible that their manipulations lead to the functional inactivation of pRb and this may phenocopy the effect of genetic inactivation of Rbf1. More importantly, our goal was to test whether the SL interactions between 11 candidates and inactivation of Rbf1 is preserved in the context of multiple oncogenic alterations and in the context of strong tumor overgrowth that was confirmed by our data. The gene discussed is PTEN; the disease is neoplasm.