Indeed, in this study, we found that exogenous Wnt5a could enhance the phosphorylation of AKT and CREB, the expression of CREB-target genes, and the growth of tumor cells that expressed low-levels of Wnt5a, indicating that Wnt5a could act in a paracrine manner for such tumors [41]. The gene discussed is CREB1; the disease is neoplasm.