In any case, as a consequence of the activation of either receptor or both of them, the signalling of NFκB, the main pro-inflammatory promoter that prevails in tumour microenvironments, could be blocked, thus reducing the levels of pro-inflammatory cytokines but increasing anti-inflammatory molecules, which could reduce the leukaemogenic environment (Figure 1(b)). Here, NFKB1 is linked to neoplasm.