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. Here, MMP12 is linked to neoplasm.