Indeed, after knocking down Tnik, the growth of xenograft CRC cells was brought to stall.251 And patients with overexpression of Tnik were manifested with poor postsurgical outcomes.253 Over 80% of CRCs have mutations in Apc,254 which makes the only molecule downstream of Apc a therapeutic target. The gene discussed is TNIK; the disease is colorectal carcinoma.