In addition, dense methylation of the TGFBI promoter is responsible for gene silencing since induction of TGFBI expression by TGF-β1 was totally lost in the tumor cells with TGFBI hypermethylation, whereas demethylating treatment with Aza-CdR resulted in the re-expression of TGFBI in these tumor cell lines. This evidence concerns the gene TGFBI and neoplasm.