In PDAC, two different studies have shown opposite conclusions, demonstrating that stromal-cleaved collagen triggers DDR1 via NF-κΒ signaling, thereby enhancing mitochondrial dynamics and tumor growth (Su et al, 2022), while the homotrimeric (i.e., intact) collagen activates DDR1/FAK/ERK in a cell-autonomous manner (Chen et al, 2022). The gene discussed is DDR1; the disease is neoplasm.