A schematic overview of the genomic and functional strategies used to identify HRD in breast tumors. HRD can arise from a variety of mechanisms, including germline and somatic mutations in HR genes such as BRCA1/2 and PALB2, as well as transcriptomic and epigenetic changes. Methods of HRD detection can be broadly categorized as (i) cause-based biomarkers, such as germline or somatic mutation testing, which are supported by strong biological rationale and extensive clinical validation but identify only a subset of HRD tumors; (ii) consequence-based biomarkers that capture genomic scarring, LOH, large-scale transitions, and telomeric allelic imbalance, which offer strong clinical validation in ovarian cancer but are often expensive and may not reflect current HR status; and (iii) dynamic biomarkers that assess real-time functional HR status, such as RAD51 foci detection and transcriptome signatures, which are promising but lack clinical validation and assay standardization. LST, large-scale state transition; TAI, telomeric allelic imbalance. *Myriad Genetics MyChoice CDx is FDA approved as a companion diagnostic for selection of patients with HRD-positive, advanced ovarian cancer who may benefit from first-line maintenance treatment with a PARPi. Although genomic scar assays are widely used in breast cancer research, no HRD assay is currently FDA approved for patient selection in breast cancer.