Thiele and colleagues discovered that the copper transporter-1 (CTR1) inhibited tumor cell proliferation through copper depletion by activating the mitogen-activated protein kinases (MAPK) pathway, which could control proliferation and division broadly, and that the chelator tetrathiomolybdate (TTM) inhibited tumor cell proliferation by significantly hindering its downstream kinase mitogen-activated protein kinase kinases 1 (MEK1) signaling [6,7]. The gene discussed is MAP2K1; the disease is neoplasm.