While the underlying mechanism by which FILIP1L inhibits β-catenin has not been determined in EOC, knockdown of FILIP1L in colon cancer cell lines led to an increase in phosphorylated AKT and GSK-3β and a decrease in phosphorylated β-catenin levels, suggesting that FILIP1L may promote β-catenin degradation by inhibiting AKT and thereby increasing GSK3β activity [73]. The gene discussed is GSK3B; the disease is colonic neoplasm.