Although KrasG12D may intrinsically drive NF-κB–CXCL5–mediated NET, our work has identified a potentially novel mechanism by which an abundant stromal molecule, collagen I, can interact with cancer cells through a targetable receptor (DDR1) to induce CXCL5 production, NET formation, and NET-mediated cancer cell invasion, even in the absence of a Kras mutation. Here, DDR1 is linked to cancer.