BRCA1 and neoplasm: Ouchi et al. [27] believed that most of the activity of IFN-γ was the result of the transcriptional response mediated by STAT1; under the synergistic effect of BRCA1 tumor suppressor and STAT1, the transcription of the IFN-γ target gene subsets could be differentially activated, and this cytokine could mediate growth inhibition.