The CRISPR-Cas9 can be exploited to induce DNA breaks, enabling correction of disease-causing mutation via the homology-directed repair (HDR) pathway. However, HDR efficiency is often limited by competition with the dominant non-homologous end-joining (NHEJ) pathway. Existing strategies to enhance HDR have yielded inconsistent results across cell types due to variations in endogenous DNA repair factor and to the different repair templates used, making universal approaches impractical. To address this challenge, we introduce the CRISPR Peptide Assisted Localization (PAL) toolkit, a modular system that customizes repair factor recruitment to specific editing conditions. CRISPR-PAL comprises a Cas9 nuclease fused to a synthetic peptide complementary to a second peptide that can be fused to a library of DNA repair effectors. We used CRISPR-PAL to identify optimal combinations of effectors tailored to specific cell types and repair templates, achieving up to a 3.1-fold increase in HDR compared to unmodified Cas9. To demonstrate its potential in challenging repair scenarios, we applied CRISPR-PAL to Fanconi anemia (FA), a disorder characterized by defective DNA repair. In FANCC mutant lymphoblastoid cells (LCLs), we used the CRISPR-PAL system to complement the missing FANCC effector, achieving over a 4-fold increase in precision score compared to unmodified Cas9 or to a direct Cas9-FANCC fusion. These results highlight CRISPR-PAL as a versatile and powerful strategy for enhancing HDR efficiency and correcting DNA repair deficiencies. By enabling precise, customizable recruitment of repair factors, CRISPR-PAL opens new avenues for addressing complex genetic disorders like FA.