Prime editing successfully corrected p47phox gene mutations in patient cells from chronic granulomatous disease (CGD), restoring neutrophil oxidative function without the genomic instability risks associated with traditional CRISPR approaches. The technique achieved precise insertion of the missing GTGT dinucleotide sequence that causes 90% of p47phox-deficient CGD cases, demonstrating functional restoration of NADPH oxidase activity in treated cells. This represents a significant advancement in gene therapy approaches for primary immunodeficiencies. Unlike conventional gene editing that creates double-strand breaks, prime editing uses a modified Cas9 nickase paired with reverse transcriptase to make targeted insertions with minimal off-target effects. The precision is particularly crucial for CGD, where patients suffer recurrent life-threatening infections due to defective immune cell function. While the study demonstrates proof-of-concept in patient-derived cells, translation to clinical therapy will require optimization of delivery methods and demonstration of long-term safety. The approach could potentially offer a curative treatment for CGD patients who currently rely on lifelong antimicrobial prophylaxis and face significant morbidity from chronic infections.