Because the effect of HSP90 inhibition on cell viability were comparable, or greater than combination of EGFR, MET, and AXL suppression (Figure 3A), and multiple RTK EGFR, ERBB2, MET, and/or AXL were simutaneously activated in individual ovarian cancer cells (Figure 1 and 2), we hypothesized that the HSP90 inhibition collectively inactivated RTK downstream intermediates including PI3-K/AKT/mTOR and RAF/MAPK signaling. The gene discussed is MET; the disease is ovarian carcinoma.