Preclinical validations have shown compelling responses to inhibition of heat-shock protein 90 (HSP90) in GIST;29–31 however, targeting HSP90 has been challenging in clinical translation,32,33 due to the toxicity resulting from concomitant on-target inactivation of various other HSP90 client proteins, beyond KIT and PDGFRA. The gene discussed is KIT; the disease is gastrointestinal stromal tumor.