As a logical extension of these findings, we examined the impact of C4.4A deficiency on bladder cancer progression in vivo using a chemically induced mouse bladder cancer model, in which oral administration of the carcinogen N-butyl-N-(4-hydroxybutyl)nitrosamine (BBN) in the drinking water induces precursor lesions that subsequently progress into malignant bladder cancer29. This evidence concerns the gene LYPD3 and urinary bladder carcinoma.