In view of the above findings, we hypothesized that MIR181A1HG in CRC cell-derived EVs may compete to bind miR373-3p through ceRNA, thereby weakening the latter’s degradation of the 3’UTR of TGFβRII, leading to the activation of TGF-β/Smads, ultimately activating HSCs. This evidence concerns the gene TGFB1 and colorectal carcinoma.