However, the function of FOXP3 in non-small cell lung cancer (NSCLC) has not been studied and the impact of FOXP3 on the Wnt/β-catenin pathway in cancers is unknown, Here, using both in vivo, in vitro models, we have demonstrated that FOXP3 is functional as an oncogenic molecule in NSCLC and have, for the first time, demonstrated that FOXP3 can act as a co-activator to facilitate the Wnt-catenin signaling pathway, inducing EMT and tumor growth and metastasis in NSCLC. The gene discussed is FOXP3; the disease is neoplasm.