In our previous study, we indicated that downregulation of FAK by high FSS is via ubiquitination mediated proteosomal degradation, and other studies have also indicated that FSS promotes several protein degradation in endothelial or cancer cells [10,46,47] Therefore, we supposed that the inhibition of total and phosphor-FAK by high FSS in TNBC cells could also be related to protein stability and degradation. The gene discussed is PTK2; the disease is cancer.