The role of LOX in optimizing PDGF signaling is further supported by studies of a LOX paralogue, the enzymatically active LOXL2, that, in an orthotopic oral cancer mouse model and human gingival fibroblasts, provided direct evidence for the oxidation of PDGFRβ promoting oral fibrosis and oral cancer [23,24]. The gene discussed is LOXL2; the disease is lip and oral cavity carcinoma.