The Zika virus outbreak in the Americas has revealed the devastating effects of the pathogen on developing fetal brains. Researchers are still trying to tease apart the precise mechanisms the virus uses to cross the placental barrier and cause microcephaly in babies. A research team led by Fanni Gergely at the University of Cambridge is now reporting that the virus relies on a protein called Musashi 1 found in fetal neural stem cells to replicate (Science 2017, DOI: 10.1126/science.aam9243). The higher the level of Musashi 1 in a neural stem cell, the more Zika virus is produced and the faster the cell dies. When the researchers reduced levels of Musashi 1 in stem cells, the pathogen could not replicate quickly. The team notes that the virus may target neural stem cells because the protein does not get produced in mature neurons. To confirm that diversion of Musashi 1 away from its typical role in brain development might lead to microcephaly, the team tracked down a family with two children who were both born with microcephaly independent of the Zika outbreak. The children had mutations in the gene for Musashi 1. Blocking the interaction between Zika RNA and Musashi 1 might reduce the pathogen’s effects on a developing brain, the researchers suggest.