While we have discovered a novel pathway whereby MC-LR impacts the interaction between M2 macrophages and CRC cells within the tumor microenvironment, additional research is necessary to comprehensively elucidate the mechanism by which TGF-β1, derived from M2 macrophages stimulated by MC-LR exposure, impedes CST3 expression in CRC cells, further facilitating CRC cell migration. Here, CST3 is linked to neoplasm.