We recently found that the selectivity of binase for tumor cells expressing theras oncogene was due to the direct interaction of RNase withthe endogenous protein KRAS [96].Investigation of activated KRAS using a non-hydrolyzable analogue of GTP(GTPγS) showed that binase prevents the exchange of GDP for GTP andreduces the interaction between RAS and the protein factors GEF and SOS1. The gene discussed is KRAS; the disease is neoplasm.