Our findings regarding the effects of ZAP knockdown or overexpression on M1 replication support the notion that ZAP acts as an anti-M1 factor in bladder cancer and are consistent with the findings of other studies regarding the antiviral role of ZAP in hepatitis B virus, human immunodeficiency virus-119,20, etc. Additionally, it is important to note that gain of ZAP function in sensitive cells did not completely abrogate the losses in cell viability induced by M1 therapy and that loss of ZAP function did not induce a significant change in the killing efficacy of M1. This evidence concerns the gene ZC3HAV1 and urinary bladder carcinoma.