Subsequent mechanistic investigations revealed that HORMAD1 activates the Wnt/β-catenin pathway by increasing the phosphorylation level of AKT at Ser473 and that of GSK-3β at Ser9 in lung cancer cells, which decreases the phosphorylation level of β-catenin at Ser33/37/Thr41, enhances the cytoplasmic and nuclear accumulation of β-catenin and its transcriptional activity, consequently promoting EMT and lung cancer growth and metastasis. This evidence concerns the gene AKT1 and lung cancer.