As illustrated in Figure 5d, LDOC1 knockdown resulted in acquired anchorage-independent growth (clonogenicity) of CGHNK2-shLDOC1 cells, and ectopic GSK-3β expression (CGHNK2-shLDOC1-GSK-3β) significantly suppressed the clonogenicity acquired after LDOC1 knockdown, suggesting that the function of GSK-3β is crucial for the anti-cancer activities of LDOC1. The gene discussed is GSK3B; the disease is cancer.