Finally, a direct interaction between the BRCT domain of BRCA1 and STAT1 has been implicated in induction of p21 and apoptosis in cancer cells in response to IFNs.40 We did not identify differences in IFN-γ receptor expression or ligand secretion between the isogenic cells lines and have attributed the augmented IFN response to an altered transcriptomic program linked to redistributed H3 acetylated marks in the presence of BRCA1 mutations. This evidence concerns the gene BRCA1 and cancer.