Exogenous Dkk3 inhibited Wnt/β-catenin signaling and cell proliferation in kidney cancer cells (8), and the cysteine-rich core domain of Dkk3 was required for dendritic cell–like differentiation from monocytes and for tumor regression, where it activated phosphorylation of GSK-3β and stat (9). The gene discussed is DKK3; the disease is neoplasm.