BMAL1 overexpression significantly inhibited cell proliferation and invasion, and induced G2/M cell cycle arrest, whereas BMAL1 knockdown promoted pancreatic cancer growth in vitro, probably by directly binding to the p53 gene promoter and thereby transcriptionally activating the downstream tumor suppressor pathway in a p53-dependent manner (152). The gene discussed is TP53; the disease is familial pancreatic carcinoma.