Fanconi anemia is a human genetic disorder with severe effects, including an increased risk of cancer and infertility. Work in animal systems has identified many factors involved in Fanconi anemia and showed that these factors function in repair of DNA. However, despite extensive analysis in mammalian somatic cell lines, in-depth studies on the germ cells, which make egg and sperm cells, have been nearly impossible in animal model systems. Now, Peter Schlögelhofer’s group at the University of Vienna, in collaboration with groups across Europe and the U.S., have used a model plant to investigate the role of a key protein, Fanconi anemia D2 protein (FANCD2), in a system where they can examine its function in germ cells. They found that FANCD2 is required for the exchange of genetic material by a previously unknown pathway that has implications for understanding this disease in humans.