<p>(A) Heat-map of cell viability changes due to HGF stimulation (log<sub>2</sub> (treated with HGF/untreated)-log<sub>2</sub> (treated without HGF/untreated)). An unbiased hierarchical clustering separated the cell population into 6 different clusters (indicated by colors on the top of heat-map). Each row indicates a treatment, and each column indicates an in silico cell. Gray to red: no change to increase due to HGF. (B) Model validation. Comparisons between experimental data (gray bars) and model predictions (red bars) after three different combinations (AKTi/MEKi, EGFRi /MEKi, and EGFRi/AKTi). Relative change of cell viability in treated-with-HGF condition to one in treated-without-HGF condition (no HGF) is reported. (C) Chord diagrams and weighted network diagrams that visualize weights between two protein nodes in the representative in silico cell <b>a</b> and <b>b</b>. The numerical data used in Fig 5 are included in the fourth sheet <a href="http://www.plosbiology.org/article/info:doi/10.1371/journal.pbio.2002930#pbio.2002930.s013" target="_blank">S1 Data</a>. AKT (PKB), protein kinase B; EGFR, epidermal growth factor receptor; ERK, extracellular receptor kinase; HGF, hepatocyte growth factor; MEK, mitogen-activated protein kinase kinase; MET (c-MET), tyrosine-protein kinase Met or hepatocyte growth factor receptor (HGFR); PI3K, phosphoinositide 3-kinase; RAF, rapidly accelerated fibrosarcoma; RAS, rat sarcoma; RAS_m, mutated RAS; RAS_w, wild-type RAS; RSK, ribosomal S6 kinase.</p
