CRISPR-mediated base editing allows precise single-base changes without double-stranded breaks, which holds great potential in gene therapy for diseases caused by single-base mutations.1 However, the clinical translation of these technologies has faced challenges, primarily due to the size limitations of delivery vectors like adeno-associated viruses (AAVs). The recent study by Hu et al. addresses these issues by developing highly efficient and compact base editors based on the Un1Cas12f1 protein.