Interestingly, in vitro and in vivo studies on pancreatic ductal adenocarcinoma (PDAC) underlined that stromal Gal-1, that is highly overexpressed by stromal fibroblasts and pancreatic stellate cells, is directly secreted in the TME and consequently establishes paracrine crosstalk with epithelial tumor cells to further trigger proliferation and invasion of cancer cells, enhance angiogenesis and inhibit immune cell infiltration (Xue et al. 2011; Martínez-Bosch et al. 2014; Orozco et al. 2018). Here, LGALS1 is linked to pancreatic ductal adenocarcinoma.