For instance, in most solid tumors, Wnt3a promoted the tumorigenesis and progression of CRC, prostate, liver, and lung cancers.68–71 Mechanistically, Wnt3a enhanced cancer cells proliferation, differentiation, migration, and self-renewal,72–74 and conversely inhibits cell apoptosis depending on activating Wnt/β-catenin.68 In leukemia, a study indicated that Wnt3a, activating Wnt/β-catenin, suppressed the proliferation of cancer cells.75 This evidence concerns the gene WNT3A and lung cancer.