Ras-like GTPases display the biological function of binary molecular switches, which are recurrent modular units in complex signaling networks. We developed a kinetic model of the K-Ras switch, which allowed uncovering molecular mechanisms underpinning specific phenotypic changes in the wt-Kras/amplification-driven Y1 tumor cells. Simulations with our K-Ras model predicted that the Y1 cells should express at least two GEFs to catalyze the transition KRas-GDP > KRas-GTP keeping high basal levels of [K-Ras-GTP]. Experimental testing validated this prediction: i) Y1 cells express two main GEFs, SOS and RasGRP4 (qRT-PCR); ii) Y1 clonal sublines selected for resistance to FGF2 (Y1FRs), showed: very low levels of K-Ras expression and negligible levels of the RasGRP4-GEF; iii) Y1 sublines knockout for the Kras gene (CRISPR-Cas9) exhibited a normal-like phenotype in culture and were not tumorigenic in Nude mice [unpublished]. We suggest that all Ras- like switches are amenable to relatively simple computational dynamic modeling.