These data confirm our initial observations that melanoma cells efficiently respond to TGF-β by a strong SMAD-specific transcriptional response [35-37], and that the lack of induction of p21 is highly gene-specific and is probably not due to a general inhibition of TGF-β signaling by SKI or SnoN, as SMAD3/4-specific transcription and induction of other TGF-β target genes, such as IL-11 or PTHrP, is intact. Here, SKI is linked to melanoma.