The cross-talk between TGFβ1, S100A8/A9 and EGF signalling results in an overall de-sensitization of cancer cells to TGFβ1 and S100A8/A9 stimuli when chronically exposed to EGF, with the exception of the apoptosis pathway, the inhibition of BAD persisting in response to the combined action of TGFβ1 and S100A8/A9 in an SMAD-4 dependent manner. This evidence concerns the gene S100A8 and cancer.