We next tested if RASON could also compete with GAP for KRAS binding and inhibit GAP-induced GTP hydrolysis in cancer cells.28,29 IP experiments in HEK293T cells showed that increasing levels of RASON overexpression dose-dependently inhibited KRAS-NF1 binding (Supplementary information, Fig. S15a), suggesting that RASON can compete with NF1 (as the representative GAP) in cells. The gene discussed is KRAS; the disease is cancer.