ATR and cancer: This is critical to the survival of cells, but more importantly to cancer cells.[6] Loss or defective DDR components are a common feature with TNBC, which often leads to a greater reliance of cancer cells on compensatory residual DDR factors for survival.[7, 8, 9] Consequently, DDR mechanisms have been of notable interest to the treatment of TNBC with inhibitors of DDR key players ATR (Ataxia Telangiectasia Mutated and Rad‐3 Related protein kinase), DNA‐PK (DNA‐dependent protein kinase), and WEE1 currently being investigated in both preclinical and clinical TNBC.[5, 10, 11, 12]