This assumption was supported not only by the anti-proliferative effects obtained through PTPRJ stimulation by a monoclonal antibody [13] but also by the discovery of synthetic PTPRJ agonist peptides able to reduce the extent of MAPK phosphorylation and, conversely, to increase cell cycle inhibitor p27Kip1 protein levels; these PTPRJ agonist peptides also reduce both cancer cell proliferation and tubulogenesis as well as trigger apoptosis of cancer cells [14, 15]. The gene discussed is PTPRJ; the disease is cancer.