"This is actually a beautiful example of evolution," says Ruth Scherz-Shouval, a postdoctoral scientist in the Lindquist lab and first author of the Cell paper. "It's recognizing that the tumor is like an organism that adheres to evolutionary principles. HSF1 has been highly conserved over time, supporting the survival of organisms ranging from yeast to human, so it makes sense that it is co-opted here. Both cancer cells and the microenvironment are sensing changes in the tumor and responding, signaling to one another to help the "organism", albeit to the detriment of the host. These are different programs, but they're both controlled by HSF1 and serve the same purpose."