We demonstrated that the formation of destruction complex condensates depends on the β-catenin accumulation of high concentrations, APC mutations prevent Axin from recruiting GSK3β and CK1α into the condensates, and Axin is related to the β-catenin nuclear translocation and its transcriptional function as a droplet, which could drive CRC initiation and progression (Fig. 6). The gene discussed is CSNK1A1; the disease is colorectal carcinoma.