In lung cancer cells, the ubiquitination level of β-catenin can be increased by FBXW2, whereas cell migration and invasion are significantly inhibited, and the dominant regulatory mechanism is the accumulation of β-cateninser552 caused by the EGFR-AKT signal pathway and ubiquitin degradation by FBXW2 (55). This evidence concerns the gene AKT1 and lung cancer.