Concurrently, PLCε−/− mice exhibited marked resistance to tumour formation in the two-stage skin chemical carcinogenesis using 7, 12-dimethylbenz[a]anthracene as an initiator and a phorbor ester 12-O-tetradecanoyl-phorbor-13-acetate as a promoter as well as to the de novo intestinal carcinogenesis on the ApcMin/+ background, which were associated with attenuation of tumor-associated inflammation exemplified by reduced expression of proinflammatory molecules9,15,16. This evidence concerns the gene PLCE1 and neoplasm.