Tumor-associated immune suppression has also been demonstrated through the upregulation of the fusion oncoprotein ETV6-NTRK3, implicated in breast cancer initiation, which simultaneously promotes STAT1 activation yet decreases STAT1 acetylation, subsequently inhibiting the acetylation of the NFκB subunit p65 to permit unchecked NFκB-driven inflammation [150]. This evidence concerns the gene STAT1 and breast cancer.