Relevant to our study, LOX activity has been reported to promote tumor migration, invasion, and metastasis via induction of the epithelial-mesenchymal transition (EMT) [38, 53–56] or activation of Src and FAK to regulate tumor behaviors through hydrogen peroxide, a byproduct produced in the process of LOX oxidizing the lysine residues of their substrates [57–60]. The gene discussed is SRC; the disease is neoplasm.