We further elucidated the downstream signaling pathway responsible for FOXP3 oncogenic function in NSCLC and found that the FOXP3-mediated tumor growth and metastasis could be, at least partly, attributed to the activation of Wnt/β-catenin signaling, which is critical for the initiation and progression of NSCLC [36, 37]. Here, FOXP3 is linked to neoplasm.