Notably, our results showed that in HCT-116 and Caco-2 cells, AdoMet significantly decreased vimentin levels and promoted the switch from N- to-E-cadherin expression, as evidenced by comparing the intensities of the corresponding protein bands in AdoMet-treated and untreated cells highlighting the ability of AdoMet to slow down CRC cell migration by inhibiting the transition from the epithelial to the mesenchymal state. The gene discussed is VIM; the disease is colorectal carcinoma.