The ability of CRISPR-Cas9 to induce dsDNA breaks can be exploited to revert a disease-causing mutation via the homology-directed repair (HDR) pathway. However, such strategies suffer from the intrinsically low frequency of HDR compared to the alternative non-homologous end-joining (NHEJ) repair pathway. Efforts to enhance HDR efficiency include the use of drugs or Cas9 fusion proteins that promote HDR and/or inhibit NHEJ. While promising, the efficacy of these approaches varies greatly across cell types, possibly related to different expression profiles of DNA repair factors. To address cell type specificity, we introduce an advanced CRISPR toolkit leveraging the dimerization ability of synthetic peptides. The CRISPR Peptide-Assisted Localization (PAL) toolkit comprises two essential elements: 1) a Cas9 nuclease fused to a synthetic peptide, and 2) a library of DNA repair effectors fused to a complementary peptide. Here, we demonstrate how CRISPR-PAL can be used to identify the most effective combination of effectors tailored to a particular cell type. Distinct nuclease and effector combinations resulted in up to a 2.5-fold increase in HDR events compared to unmodified Cas9 across diverse cell types. Furthermore, dimerization in CRISPR-PAL enabled the use of novel combinations that were unamenable through mere overexpression of effectors. Ongoing experiments examine CRISPR-PAL's effectiveness in correcting Fanconi anemia-specific mutations by augmenting missing effectors at the target site. We anticipate that the CRISPR-PAL toolkit will be instrumental in the development of tailored genome editing solutions with broad therapeutic applications.