Cancer‐associated fibroblasts (CAF) also drive PNI in pancreatic cancer.[37] Enhanced glycolysis in CAFs drives the formation of a high‐lactate tumor microenvironment that favors cancer progression.[37] Coincidentally, in an acetaminophen‐induced liver injury model, the intercellular crosstalk between MMP12+ macrophages was found to be sustained by enhanced glycolysis.[38] This observation led us to speculate that the SRC‐1‐mediated secretion of MMP12 from macrophages may also be associated with glycolytic reprogramming in CAF‐mediated PNI. This evidence concerns the gene MMP12 and familial pancreatic carcinoma.