MACC1 knockdown effectively inhibited proliferation and promoted apoptosis of lung adenocarcinoma cells by regulating the β-catenin pathway (including c-myc) [47], and DBC1 (BMP/retinoic acid inducible neural specific (1), which play a key role in CRC progression through Wnt/β-catenin-MACC1 signaling axis [48]. The gene discussed is MYC; the disease is lung adenocarcinoma.