The mutant strain revealed that 1) FGFR2 activation significantly increases the incidence of TNBC formation, 2) tumorigenesis is accompanied by BRCA1 downregulation and is accelerated by targeted BRCA1 deletion, 3) FGFR2 activation upregulates PD‐L1 associated with pSTAT3, and 4) FGFR2 inhibition and anti‐PD‐1/anti‐PD‐L1 blockade markedly inhibit tumor growth. The gene discussed is BRCA1; the disease is neoplasm.