This suggests that the IFNα pathway is not saturated at basal levels in TN-IBC indicating three things: (1) TN-IBC may still be able to respond to exogenous IFN treatment in both a pro- and anti-tumor manner depending on concentration; (2) this pathway may be stimulated on a basal level to confer autocrine signaling to the tumor, promoting increased aggression by mediating the levels of STAT1, STAT2, and IRF9; or (3) TN-IBC cells may not be sensitive to autocrine IFNα signaling. This evidence concerns the gene STAT1 and neoplasm.