To determine whether chemogenetic inhibition of CaMKIIα‐positive neurons in the VAL modulates CRS‐induced hyperalgesia, we bilaterally delivered the Gi‐coupled DREADD construct AAV‐CaMKIIα‐hM4Di‐mCherry into the VAL of mice 7 days before CRS initiation, allowing viral expression prior to multimodal behavioral assessments (Figure 2A–C). This evidence concerns the gene CAMK2A and congenital rubella syndrome.