Whereas mutant APC is also capable of LLPS, the assembled condensates cannot recruit GSK3β and CK1α, which results in the inability to phosphorylate β-catenin, allowing β-catenin to accumulate in the cytoplasm, further enhancing the transcriptional activity of the Wnt/β-catenin signaling pathway, and ultimately leading to colorectal cancer development (17, 110, 111). Here, APC is linked to colorectal cancer.