Recently, Whitehead Institute researchers found that increased expression of a specific gene promotes metastasis and death in patients with breast, colon and lung cancers. This finding will not only help scientists identify gene expression profiles to predict patient outcomes and treatment response, but could also guide the development of therapies for many types of cancer. In normal cells, various stresses including heat, hypoxia, and toxins activate heat shock factor 1 (HSF1), leading to increased expression of so-called heat shock or chaperone proteins to maintain stressful intracellular homeostasis. Scientists already knew that many cancer cells have higher levels of chaperone proteins, which are important for tumor cell survival and proliferation. Now, however, researchers report that HSF1 not only increases cancer chaperone protein expression, but also regulates a fairly broad range of malignant behaviors in tumor cells. HSF1 activity promotes the development of the three most prevalent cancer types: breast, lung, and colon cancer. In addition to confirming that this gene activation program is different from that of heat shock proteins, the researchers found that in many tumors it becomes active in almost all tumor cells. This suggests that it does not simply drive HSF1 activity in situations where tumors experience environmental stress, but rather connects to a core region where HSF1 activates cancer cells, promoting a unique gene regulatory program that allows tumors to acquire an aggressive phenotype. This suggests that HSF1 itself may be a potential therapeutic target.