Dysfunction of BRCA1 resulted in the accumulation of ALDH1‐positive/ER‐negative stem/progenitor cells in mammary tissue,[31] while down‐regulation of BRCA1 resulted in significant increase of the breast cancer stem cell ‐like populations.[32] However, another HR regulator RAD51 upregulated in ALDH+ BTICs and mediated BTICs resistant to PARP inhibitors[33, 34] suggesting that increased HR repair efficiency bypassed BRCA1 function might mediate BTICs resistant to PARPi. Here, PARP1 is linked to breast carcinoma.