In parallel, it is mainly the N219 site whose glycosylation leads to STAT3 and STAT1 activation, with some roles also attributed to the N192 and N200 sites (depending on the cell type), consequently giving rise to pro-metastatic phenotypes in the cancer cells upon PD-L1 expression (as found in Figure 1, Figure 2, Figure 3 and Figure 4). This evidence concerns the gene STAT3 and cancer.