While loss of the tumor suppressor APC is the characteristic mutation resulting in Wnt-pathway activation in CRC etiology, cancer therapeutic development targeting the Wnt pathway is focused on downstream mediators including tumor necrosis factor receptor-associated factor (TRAF) and NCK-interacting protein kinase (TNIK), an essential regulator of the TCF4/β-catenin complex [110]. The gene discussed is TNIK; the disease is colorectal carcinoma.