Reports suggest that PARP inhibitors induce replication stress and enhance genomic instability.39,40 It has also been established that PARP inhibitor toxicity in HR-deficient cancer cells is in part due to the progression through mitosis with accumulated genomic aberrations.41 Since autophagy is also known to play a vital role in genome maintenance,42,43 we sought to know whether de novo resistance to PARPi could be linked to autophagy-mediated genome maintenance in BRCA1-WT breast cancer cells. The gene discussed is BRCA1; the disease is breast carcinoma.