PARP inhibitors have emerged as promising anticancer agents, particularly in BRCA1- and BRCA2-deficient tumors. This review summarizes the structure, function, and biological roles of PARP enzymes, with a focus on PARP1. PARP1 is activated by DNA damage and plays a critical role in DNA repair, particularly in base excision repair (BER) and homologous recombination. PARP1 hyperactivation leads to the synthesis of poly(ADP-ribose) (pADPr), which can cause metabolic cell death, parthanatos, and genomic instability. PARP inhibition is particularly toxic in BRCA-deficient cells, as these cells are unable to efficiently repair DNA damage through homologous recombination. This synthetic lethality has led to the development of PARP inhibitors as targeted therapies for BRCA-mutated cancers. PARP inhibitors work by depleting NAD+ and inhibiting PARP1 activity, which is essential for DNA repair. Third-generation PARP inhibitors are more potent and specific than earlier ones and have shown promise in clinical trials. These inhibitors can be used in combination with DNA-damaging agents to enhance their therapeutic effect. However, long-term use of PARP inhibitors may have unintended consequences, such as secondary malignancies, and their effects on cardiovascular and neurological health need to be carefully evaluated. The PARP family includes several enzymes, with PARP1 being the most well-characterized. Other members, such as PARP2, PARP4, and tankyrase 1 and 2, also play roles in DNA repair and other cellular processes. Recent studies suggest that tankyrase inhibitors may be useful in targeting BRCA-deficient tumors without inhibiting PARP1. However, the exact roles of these enzymes in DNA repair and cancer remain to be fully understood. Despite significant progress, many questions remain about the biology of PARPs and their role in cancer. Further research is needed to understand the mechanisms of PARP inhibition, its effects on DNA repair, and its long-term safety. The development of PARP inhibitors as a therapeutic strategy is promising, but careful evaluation of their efficacy and safety is essential.PARP inhibitors have emerged as promising anticancer agents, particularly in BRCA1- and BRCA2-deficient tumors. This review summarizes the structure, function, and biological roles of PARP enzymes, with a focus on PARP1. PARP1 is activated by DNA damage and plays a critical role in DNA repair, particularly in base excision repair (BER) and homologous recombination. PARP1 hyperactivation leads to the synthesis of poly(ADP-ribose) (pADPr), which can cause metabolic cell death, parthanatos, and genomic instability. PARP inhibition is particularly toxic in BRCA-deficient cells, as these cells are unable to efficiently repair DNA damage through homologous recombination. This synthetic lethality has led to the development of PARP inhibitors as targeted therapies for BRCA-mutated cancers. PARP inhibitors work by depleting NAD+ and inhibiting PARP1 activity, which is essential for DNA repair. Third-generation PARP inhibitors are more potent and specific than earlier ones and have shown promise in clinical trials. These inhibitors can be used in combination with DNA-damaging agents to enhance their therapeutic effect. However, long-term use of PARP inhibitors may have unintended consequences, such as secondary malignancies, and their effects on cardiovascular and neurological health need to be carefully evaluated. The PARP family includes several enzymes, with PARP1 being the most well-characterized. Other members, such as PARP2, PARP4, and tankyrase 1 and 2, also play roles in DNA repair and other cellular processes. Recent studies suggest that tankyrase inhibitors may be useful in targeting BRCA-deficient tumors without inhibiting PARP1. However, the exact roles of these enzymes in DNA repair and cancer remain to be fully understood. Despite significant progress, many questions remain about the biology of PARPs and their role in cancer. Further research is needed to understand the mechanisms of PARP inhibition, its effects on DNA repair, and its long-term safety. The development of PARP inhibitors as a therapeutic strategy is promising, but careful evaluation of their efficacy and safety is essential.