Background HR deficiency (HRD) may be exploited through use of DNA-damaging chemotherapy and/or PARP inhibitors (PARPi). The current biomarker to infer HRD in breast cancer (BC) is a germline pathogenic variant (PV) in BRCA1/2 (gBRCAm). This biomarker strategy misses a significant proportion of HRD BC. We analysed the HR status of an enriched cohort of platinum-responsive aTNBC on the DORA study. Methods Between Feb 2019, and Dec 2020, 45 patients (pts) were enrolled to receive maintenance olaparib (O) +/- durvalumab (D). HRD testing using Pillar Biosciences oncoReveal™ HRD Panel was performed on archival tissue. This panel detects SNVs and indels in 33 HR related genes. Quantitation of BRCA1 and RAD51C promoter methylation assessed using oncoReveal™ BRCA1 & RAD51C Methylation Panel. Median progression free survival (mPFS) by HR status was compared using log-rank test. Results Of the 45 pts, 40 had available samples for HRD testing. gBRCAm were reported from medical history: 15 (37.5%) gBRCA unknown, 17 (42.5%) gBRCA wildtype, 8 (20%) gBRCAm. 21 (52.5%), harbored any HR alterations (HRD). OncoReveal™ panel identified 8 BRCA1 (1 FANCA co-mutation), 1 BRCA2, 2 PALB2, 1 BRIP1, 1 RAD51D PV. Mutually exclusive to BRCA PV, 9 were identified to have BRCA1 promoter hypermethylation, 5 classified as highly methylated. 1 tumor with partial BRCA1 hypermethylation had concurrent highly methylated RAD51C. 1 BRCA1 highly methylated tumor had a co-mutation with BRIP1. The mPFS of pts with HRD vs. no HRD was 7.8 months (m) (3.9 - not estimable) vs. 2.1 m (1.9 - 3.4), p=0.002. The association between mPFS and HRD did not vary by maintenance therapy. The mPFS of O pts (HRD n=9 vs. no HRD n=10) is 7.8 vs 1.9 m HR 0.3; 0.11-0.8 and of O+D pts (HRD n=12 vs. no HRD n=9) is 7.4 vs 3.3 m HR 0.34; 0.12-1.0. 11 of the 21 pts with HRD were on maintenance therapy for >6 months vs. 3 of the 19 pts without HRD. Conclusions BRCA1/RAD51C promoter hypermethylation and mutations are mutually exclusive with similar proportions identified in this enriched cohort of aTNBC. Current companion diagnostic for PARPi therapy underestimates the proportion of BC with HRD. Testing for BRCA1/RAD51C hypermethylation to guide therapies is worthy of further exploration.