Nevertheless, the strong LPS-induced cytosolic p62 signalling observed is reminiscent of that reported in keratinocytes45 where although TLR-signalling promotes p62-dependent autophagy to negatively regulate inflammation, p62, in keeping with its ability to activate NF-κB in autophagy-defective tumour cells46, 47, also promotes NF-κB activation and consequent inflammatory responses. The gene discussed is NFKB1; the disease is neoplasm.