These findings also suggest that cancers driven by FGFR3 overexpression (as FGFR3 appears to be a better client compared with other FGFRs), or by FGFR3 mutations that further destabilize kinase structure, might be particularly worthwhile targets for exploration of Hsp90 and FGFR kinase inhibitor combinations as potential synergistic molecular therapies aimed at overcoming clinical drug resistance to kinase inhibitors as single agents. The gene discussed is FGFR3; the disease is cancer.