The base excision repair (BER) is the primary damage repair pathway for repairing most of the endogenous DNA damage including oxidative base lesions, apurinic/apyrimidinic (AP) sites, and single-strand breaks (SSBs) in the genome. Repair of these damages in cells relies on sequential recruitment and coordinated actions of multiple DNA repair enzymes, which include DNA glycosylases (such as OGG1), AP-endonucleases (APE1), DNA polymerases, and DNA ligases. APE1 plays a key role in the BER pathway by repairing the AP sites and SSBs in the genome. Several methods have been developed to generate a map of endogenous AP sites or SSBs in the genome and the binding of DNA repair proteins. In this chapter, we describe detailed approaches to map genome-wide occupancy or enrichment of APE1 in human cells using chromatin immunoprecipitation followed by next-generation sequencing (ChIP-seq). Further, we discuss standard bioinformatics approaches for analyzing ChIP-seq data to identify APE1 enrichment or binding peaks in the genome.