In a paper published in Cell Host and Microbe, Anna Cliffe identifies how activation of JNK in response to neuronal stress triggers changes to the HSV chromatin and reactivation from latency. While stress is generally considered to be a factor that triggers HSV reactivation from latency, the molecular mechanisms were unknown. Cliffe et al. show that a neuronal stress pathway involving JNK activation is crucial for HSV reactivation. They found that JNK signaling induces histone phosphorylation on repressed viral promoters, therefore linking cell stress with initial stimulation of viral gene expression.