Mom’s eyes and dad’s tumor? Cancer is due to genetic defects, some of which can be hereditary. The gene variant rs351855, for example, occurs in one in two cancer patients. It supports the growth of a variety of tumors that are aggressive and difficult to treat. A team headed by Axel Ullrich from the Max Planck Institute of Biochemistry in Martinsried identified the gene variant a decade ago. The same laboratory has now succeeded for the first time in showing that the defect exposes an otherwise hidden binding site on the FGFR4 receptor. In a previously unknown interaction, growth factor STAT3, which promotes cancer, binds to the exposed site. The STAT3 signaling cascade can be efficiently blocked. For the first time, this could provide a promising therapeutic approach for many cancer patients. At the same time, it represents an important step towards personalized medicine. The paper was published in Nature.