Our current results are in agreement with this mechanism as the application of pan-SFK pharmacological inhibitors increased the transcriptional activity of the AP-1 complex, as measured by the phosphorylation status of c-Fos (Figure 2A and 2B) and its recruitment to the AP-1 binding site of the human CLDN2 promoter in breast cancer cells (Figure 2C). This evidence concerns the gene JUN and breast carcinoma.