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The most predominant drivers of breast cancer therapeutic resistance are summarized in Figure 4, which include a complex interplay of genetic factors (e.g., PTEN, TP53 mutations, HER2 amplification), epigenetic mechanisms (e.g., DNMT-mediated methylation, EZH2-driven H3K27me3), ncRNAs (e.g., HOTAIR, miR-21 with m6A modifications), apoptosis evasion (e.g., Bcl-2 upregulation), robust DNA repair (e.g., HR, NHEJ), and an immunosuppressive TIME (e.g., T cell exhaustion, MDSC infiltration, PD-L1 overexpression), particularly in TNBC and HER2-positive subtypes, highlighting multifaceted targets for precision oncology

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S., Lund, A., Vilsboll, T., Knop, F