Scientists achieved precise single-letter DNA correction in living mouse brains, successfully reversing autism-like behaviors, cognitive deficits, and motor problems caused by mutations in the CHD3 gene. Using a custom adenine base editor delivered via dual adeno-associated virus vectors, researchers corrected the pathogenic R1025W variant across cortical and hippocampal regions with 85% efficiency and minimal off-target effects. The intervention restored normal CHD3 protein levels and improved social communication, learning, and coordination in mice modeling Snijders Blok-Campeau syndrome. This represents a watershed moment for neurodevelopmental medicine, marking the first successful in vivo correction of a chromatin remodeling disorder through base editing. Unlike traditional gene therapies that add functional copies, this approach fixes the underlying genetic error with single-nucleotide precision. The implications extend far beyond CHD3 disorders—thousands of neurodevelopmental conditions stem from single-base mutations in genes controlling brain development and function. The researchers' success with nonhuman primate delivery further validates clinical feasibility. However, questions remain about optimal treatment timing, long-term safety, and whether correction must occur during critical developmental windows. The work establishes postnatal brain editing as a legitimate therapeutic paradigm, potentially transforming treatment of previously intractable genetic neurological conditions.