Breast cancer can evolve over time, leading to increased genomic complexity and heterogeneity, which may impose selective pressures and result in differential responses to therapies.119 Detailly, breast cancer cells mimic the anti-inflammatory mechanism of central nervous system to evade antitumor immunity, which is dependent on the immunological synapse.120 Carrying lower clonal heterogeneity and neoantigen loads, TNBC cells achieve immune escape via Lgals2-CSF1-CSF1R axis,121 which is also a specific mechanism in breast cancer immune escape. The gene discussed is CSF1R; the disease is breast carcinoma.