Similar intracellular factors are reviewed in Table 3, and despite the absence of sufficient evidence, these factors could have the potential to overcome resistance to interferon-based drugs, e.g., BRCA1 (BRCA1 DNA repair associated), a famous target for cancer therapy, significantly upregulates JAK1 expression and interacts with STAT1 dimers, which govern the IFN-dependent anti-proliferative response of breast cancer [96]. This evidence concerns the gene JAK1 and breast carcinoma.