To explore whether HSCs activated by MIR181A1HG in CRC cell-derived EVs could promote CRLM, LX2 cells were first cocultured with EVs derived from HT29/RKO cells that had been pretransfected with MIR181A1HG overexpression or knockdown constructs. This evidence concerns the gene MIR181A1HG and colorectal carcinoma.