To give a further biomedically relevant example, the tumor suppressor p16INK4a is the master regulator for a glycan-based effector route to drive pancreatic carcinoma cells into programmed cell death: the underlying caspase-9 activation is achieved by clustering of α5β1-integrin and galectin-1 on the cell surface, a process favored by their concerted upregulation and the increase of galectin-1-suited integrin glycosylation through reducing α2,6-sialylation of its N-glycans [33,34]. This evidence concerns the gene LGALS1 and exocrine pancreatic carcinoma.