Since the inhibition of a single heat shock protein such as Hsp90 inevitably leads to the compensatory upregulation of other heat shock proteins such as Hsp70 and Hsp27, targeting Hsf1 instead of the individual chaperones separately is potentially more therapeutically effective, as inhibition of Hsf1 could in theory abolish the ability of a cancer cell to activate the whole heat shock response during cellular stress. The gene discussed is HSF1; the disease is cancer.