In preclinical models, Col I remodelling modulated tumour growth and metabolism through a DDR1–NF-κB–p62–NRF2 cascade that is activated by cCol I and inhibited by iCol I. The activation of DDR1 by collagens and downstream activation of NF-κB have been described before14,16. The gene discussed is NFKB1; the disease is neoplasm.