The article by Chatterjee and Walker provides an in-depth review of the mechanisms of DNA damage, repair, and mutagenesis. DNA damage can be categorized into endogenous and exogenous sources, with endogenous damage arising from chemical reactions within cells and exogenous damage from environmental, physical, and chemical agents. Endogenous damage includes replication errors, base deamination, abasic sites, oxidative DNA damage, and DNA methylation. Exogenous damage encompasses ionizing radiation, ultraviolet (UV) radiation, alkylating agents, aromatic amines, polycyclic aromatic hydrocarbons (PAHs), other reactive electrophiles, toxins, and environmental stresses. The DNA damage response (DDR) is a critical mechanism that senses and repairs DNA damage, involving lesion-specific sensor proteins and chromatin remodeling. Key repair pathways include base excision repair (BER), nucleotide excision repair (NER), mismatch repair (MMR), homologous recombination (HR), and non-homologous end joining (NHEJ). These pathways collectively ensure genomic stability and prevent mutations. Deviations in these pathways, such as those observed in cancers, can lead to genome instability and disease progression. The review highlights the importance of understanding these mechanisms for the regulation of genotoxic agents and the prevention of human diseases.The article by Chatterjee and Walker provides an in-depth review of the mechanisms of DNA damage, repair, and mutagenesis. DNA damage can be categorized into endogenous and exogenous sources, with endogenous damage arising from chemical reactions within cells and exogenous damage from environmental, physical, and chemical agents. Endogenous damage includes replication errors, base deamination, abasic sites, oxidative DNA damage, and DNA methylation. Exogenous damage encompasses ionizing radiation, ultraviolet (UV) radiation, alkylating agents, aromatic amines, polycyclic aromatic hydrocarbons (PAHs), other reactive electrophiles, toxins, and environmental stresses. The DNA damage response (DDR) is a critical mechanism that senses and repairs DNA damage, involving lesion-specific sensor proteins and chromatin remodeling. Key repair pathways include base excision repair (BER), nucleotide excision repair (NER), mismatch repair (MMR), homologous recombination (HR), and non-homologous end joining (NHEJ). These pathways collectively ensure genomic stability and prevent mutations. Deviations in these pathways, such as those observed in cancers, can lead to genome instability and disease progression. The review highlights the importance of understanding these mechanisms for the regulation of genotoxic agents and the prevention of human diseases.