Since chronic fibrosis is not only a consequence but also a risk factor for cancer—as suggested by clinical evidence that IPF is an independent risk factor for lung cancer [112] or that fibrosis induced by epidermolysis bullosa is strongly associated with patient predisposition to develop squamous cell carcinoma [113]—effective antifibrotic therapy, targeting the ATX/LPA axis, could offer the advantage of combining the antifibrotic effect with preventive action against possible fibrosis-induced tumors. The gene discussed is LPA; the disease is cancer.