The article reviews the mechanisms by which antibiotics kill bacteria, focusing on the multi-layered effects of drug-target interactions and the cellular responses that contribute to cell death. It highlights the complex biochemical and genetic pathways involved, including the inhibition of DNA replication, RNA synthesis, cell wall synthesis, and protein synthesis. The review also discusses the role of the SOS response and oxidative stress in antibiotic-induced cell death, and explores new insights gained from network biology studies. Additionally, it examines the potential of synthetic biology to develop novel antibacterial therapies, such as using engineered gene circuits and bacteriophage delivery systems to enhance antibiotic efficacy. The authors emphasize the importance of understanding these mechanisms to combat the growing threat of drug-resistant bacterial infections.The article reviews the mechanisms by which antibiotics kill bacteria, focusing on the multi-layered effects of drug-target interactions and the cellular responses that contribute to cell death. It highlights the complex biochemical and genetic pathways involved, including the inhibition of DNA replication, RNA synthesis, cell wall synthesis, and protein synthesis. The review also discusses the role of the SOS response and oxidative stress in antibiotic-induced cell death, and explores new insights gained from network biology studies. Additionally, it examines the potential of synthetic biology to develop novel antibacterial therapies, such as using engineered gene circuits and bacteriophage delivery systems to enhance antibiotic efficacy. The authors emphasize the importance of understanding these mechanisms to combat the growing threat of drug-resistant bacterial infections.