A study in PDAC showed that collagen components can regulate PDAC energy metabolism, macrophage phagocytosis, and tumor growth via the Discoidin Domain Receptor Tyrosine Kinase 1 (DDR1)-mediated signaling axis, the collagen type I (Col1)-DDR1-NF-κB-NRF2 mitochondrial biosynthetic pathway, by activating the DDR1 receptor [131], providing a theoretical basis for targeted intervention in this pathway. The gene discussed is NFKB1; the disease is neoplasm.