ATR also known as ataxia-telangiectasia is a serine/threonine kinase and DNA damage sensor, activating cell cycle checkpoint signaling upon DNA stress. ATR plays a crucial role in the cellular response to DNA damage, particularly in the activation of cell cycle checkpoints. ATR phosphorylates key proteins involved in the DNA damage response, such as checkpoint kinase CHK1 and tumor suppressor BRCA1, making ATR vital for maintaining genomic stability. ATR is primarily located in the nucleus, where ATR forms intranuclear foci in response to DNA damage or replication stress, highlighting ATR′s importance in cellular repair mechanisms. ATR is essential for early embryonic development, underscoring ATR′s significance in both normal cellular function and the prevention of diseases associated with genomic instability.