Because cell death induced by the CD24 cross-linking antibody was shown previously to be through mitochondrial regulation (reactive oxygen species generation and/or Bcl-2 inhibition), we currently investigating whether in IRSOE/TNBC/TICs, mitochondrial regulation could be another possible combinatorial therapy in addition to IRIS inhibitor + anti-CD24 blocking antibody to benefit breast cancer patients with localized BRCA1-low/IRISOE/TNBCs. The gene discussed is BRCA1; the disease is breast carcinoma.