Our hypothesis that vimentin is a key factor integrating EMT, neoplastic progression and resistance to HDACis in the colon (Fig. 1) is supported by the literature cited above, the strong link between vimentin‐mediated EMT and drug resistance 36, and our gene expression data, according to which butyrate‐resistant CRC cells consistently up‐regulate vimentin within the context of a p300‐deficient, EMT‐like phenotype that exhibits suppressed expression of E‐cadherin (14, 16, unpublished data). This evidence concerns the gene VIM and colorectal carcinoma.