JAK SIGNALING, STIMULATED BY INTERFERON AND OTHER GROWTH FACTORS AND RELEVENT CYTOKINES CANNOT DO ITS WORK UNTIL IT REACHES TRANSCRIPTION FACTORS OF WHICH AMPLIFICATION IS TRANSLATED IN MODULATION OF REGULATORS OF PROMOTOR GENES.
This links the JAK signaling Pathway to the STAT.
In a recent article by Lee et al.,
"Acetylation of STAT3 is crucial to Methylation of tumor suppressor gene promoters", the authors, tying their work to Breast cancer, state: "Furthermore, reduction of acetylated STAT3 in triple-negative breast cancer cells leads to demethylation and activation of the estrogen receptor-α gene, sensitizing the tumor cells to antiestrogens. Our results also demonstrate a correlation between STAT3 acetylation and methylation of estrogen receptor-α in melanoma, which predicts melanoma progression. Taken together, these results suggest a role of STAT3 acetylation in regulating CpG island methylation,"
 These could be used as further supporting evidence for our proposed combination of mTOR with Interferon in triple negative Breast Cancer.
There is another important issue raised here that depression in STAT level may activate Estrogen receptor with a possibility of causing Breast cancer or progression thereof!

1.Is STAT genetic amplification a predictor of Hormonal manipulation response to intervention
2. Is activation of these STAT an effective prevention therapy in patient with BRCA positivity, in otherway should STAT status be assessed in patient participating in prevention with Tamoxifen and Raloxifen to really measure and understand subset variances.
3.Does inclusion of mTor and Cytokines break the need of testing ER positivity, or at least weaken the need of such determination so long as the STAT is depressed?
4.Role of Deacetylation of STAT in Breast Cancer/Target of therapy.  De-Methylation of promoter gene to stop their silencing.?