Reticker-Flynn and Bhatia have shown that galectin-3 contributes to the formation and establishment of a pro-tumorigenic metastatic niche. The authors analysed the expression of galectin-3 in the liver of a mouse model of metastatic lung adenocarcinoma and found that it was expressed in a population of myeloid cells, which are mobilized in response to soluble factors secreted from cancer cells. Further experiments showed that metastatic cancer cells adhere to galectin-3 through increased presentation of galectin-3 carbohydrate ligand (the Thomsen–Friedenreich antigen), which is mediated by aberrant glycosyltransferase.