You probably remember the 2015 sky-high rates of infant microcephaly in Brazil, ringing alarm bells of a new and terrifying epidemic. The culprit was determined to be a maternal infection with the Zika virus causing little more than a mild headache in mom, all the while dangerously decelerating brain development in the fetus. Though it made little sense to attribute these discordant outcomes to a single pathogen, the correlation was undeniable. It has since been discovered that a primary cellular gateway for Zika is the Axl protein, heavily expressed on human glial cells (i.e., brain stem cells). Glial cells act almost exclusively during...you guessed it...fetal development, explaining the vastly discordant symptoms in mom and baby. Yet they occasionally have another more notorious part to play in adults, namely enabling glial malignancies such as glioblastoma multiforme (GBM) to evade traditional oncologic therapies. Do you see where we’re going with this yet? A report this week demonstrates an oncolytic Zika virus has been used to successfully treat GBM in mice. It appears the answer to one devastating disease just may be hiding in the mechanism of another.