They play pro-tumour roles, through the production of some cytokines and growth factors, and through the deposition of collagen, which favours the tumour process in more ways than one: it stimulates the growth and the metabolism of neoplastic cells through the activation of the discoidin domain receptor 1 (DDR1)–NF-κB–p62–NRF2 signalling; creates excessive fibrosis, which in turn causes defective vasculature and hypoxia, resulting in the selection of apoptosis- resistant tumour clones; and hinders the penetration of anticancer effector cells (CTLs, etc.)(6–8). Here, NFKB1 is linked to neoplasm.